cardiology Flashcards
what does the myocardium do and what happens if it goes wrong
pump
heart failure
what does the valves do and what happens if it goes wrong
heart failure
endocarditis
coronary artery disease
whats important
very important to make distinction between stable coronary disease (largely silent, angina) and unstable - causes sudden death, heart attacks etc
risk factors for coronary artery disease
smoking high cholesterol high bp diabetes overweight poor diet lack of physical activity other atherosclerotic conditions - stroke/ peripheral vasc disease fh genetics male sex age
what is a MI
occurs when atherosclerotic plaque in coronary art ruptures, triggering thrombus formation
this causes permanent death of some myocardium (unlike angina)
in an acute MI - its the thrombus that kills - treating the clot is impportant
the rf + plaque can wait for a few days
how can you tell if someone has coronary artery disease
exercise ECG - easy but inaccurate (50% of women will be positive even when theyre not)
myocardial perfusion scan - slightly more accurate (done at rest + stress)
angiography - either CT (chronic) (best test) or invasive angiography (for possible acute MI) in case stent needed
limitations of CT angiogram
if calcium cant see how intense plaque is
not invasive
mx of coronary art disease
main goal - prevent future MI, stroke + death
lifestyle modificaton - stop smoking, take more exercise, eat heart healthy diet (5-7 veg/fruit/low processed food, oily fish, olive oil, nuts/seeds), lose weight
cholesterol loweing - statin
antiplatelets - usually aspriin
address risk factors - BP, diabetes
these improve prognosis but do not reduce angina frequency
mx of coronary art disease
main goal - prevent future MI, stroke + death
lifestyle modificaton - stop smoking, take more exercise, eat heart healthy diet (5-7 veg/fruit/low processed food, oily fish, olive oil, nuts/seeds), lose weight
cholesterol loweing - statin
antiplatelets - usually aspirin
address risk factors - BP, diabetes
these improve prognosis but do not reduce angina frequency
if CAD is causing angina (stable) .. mx..
no need to treat if not bothersome
meds to reduce attacks - GTN, BB, CCB, nicorandil, ivabradine, ranolazine
meds not working/se - stenting or coronary artery bypass grafting
these improve angina but do not improve prognosis
key investigations of MI
ECG - if shows ST elevation most likely STEMI, if normal or shows other changes (ST depression, T wave inversion) - may be NSTEMI or trapped wind
serum troponin measurement - in both STEMI and NSTEMI serum trop will be raised - but treat as MI until results back. If this isn’t raised its not an MI
mx of STEMI + NSTEMI
immediate dual antiplatelet therapy (aspirin + Ticagrelor/ Prasugrel/clopidogrel) + pain relief.
paramedics usually give aspirin and opiates
oxygen should be avoided + nitrates are useless
anticoag for 24-72 hours - heparin, fondaparinux or similar
both STEMI and NSTEMI should have angiography and if poss stenting, STEMI immediately, NSTEMI within 72 hours or sooner if comps
secondary prevention - dual antiplatelet therapy for a year then aspirin alone, statin, BB for a year, ACEi, treatmentof any comp (HF, arrhythmia)
cardiac rehab - exercise, diet, smoking cessation
when in exam how do you write ECG
12 lead ECG
Asymptomatic brady do you pace?
no
ix of intermittent arrhythmias (brady or tachy)
diagnosis made by ECG at time of symptoms - mutliple 24hr recordings, home recorders, smartphone apps, implanted loop recorder
others to look for causes - echo for HF, valve disease, angio for coronary art disease, fam screening/testing for genetic conditions
treatment of heart failure
prodominantly medical - drugs
correction of other causes - anaemia, alcohol,thyroid dysfunction
ACE i, BB, aldosterone antagonists (spironolocatone, eplerenone), diuretics, ivabradine
manage comps - arryhthmia
some sort of heart failure patients benefit from cardiac resyncronisation therapy
mx for valve disease
limited role for meds
mainly loop diuretics
BB for aortic stenosis
HF meds if LV systolic function impaired - probs means valve needs replacing already
treat AF as normal if present - common with mitral valve
definite treatment with valve repair, replacement, or TAVI (transcather aortic valve implantation) for aortic stenosis
explain ECG ‘leads’
these are views of the heart
given 12 on the ECG strip
they come from 10 electrodes on the body
4 limb electrodes = 6 limb leads and view the heart in a vertical plane I, II, III, AVR, AVF, AVL
6 chest electrodes = 6 chest leads and look at the heart on the horizontal plane, V1-6.
what to remember when recording a 3 lead ECG
this is just the limb leads ride your green bike - clock wise round body from right arm R = red right arm Y = yellow left arm G = green left leg B = black right leg
which electrodes on ECG must be accurate?
the chest leads - must be accurate and standardised every time -
- V1 + 2 4th intercostal space either side of sternum
- V4 midclavicular line 5th intercostal space
- V3 in between them in a diagonal line
- V5 - anterior axillary line over 5th rib
- V6 - midaxillary line in line with V5
limb leads can be placed literally anywhere on the limbs - but try for somewhere bony and not hairy
what machine settings do you need for ECG machine for a normal reading
paper speed - 25mm/sec
voltage calibration - 1mV causes an upward deflection of 1cm
always have date +time and patients name at LEAST
write the patients symps and BP on ECG
where is the sinoatrial node
right atrium
what direction do I, II, III, AVR, AVF, AVL look at the heart from
AVR - right shoulder AVF - directly upwards AVL - left shoulder I - direct left II - left bottom corner III - right bottom corner
what does these look at:
- p wave
- PR interval
- QRS complex
- ST segment
- T wave
- p wave - electrical activation aka depolarisation of atrium
- PR interval - time taken for electrical impulse to spread from atria to ventricles through av node and bundle of His
- QRS complex - the impulse spreading throughout the ventricles = ventricular contraction. should not be more than 3 small squares
- ST segment - when ventricles are completely activated
- T wave - is the repolarisation, ventricles returning to resting state
how to interpret ECG steps
look at patient - unwell? well?
take pulse and BP - what are you expecting to see
immediately look for any clear scary abnormalities and get help if necessary
‘RRPWQST’
R - rate - for speed if <3 large squares between each QRS complex is >100bpm and >6 = <50bpm
R - rhythm - reg or irreg
P - p wave - always present? = sinus rhythm. if cant see p wave always then atria not activated normally, if more than 1 p wave before every QRS then ventricles are not activated normally = heart block
W - width - QRS <3 small squares, if not its slow
Q - any deep Q waves present? if so shows old myocardial infarction
S - ST segment - depressed (ischaemia) or elevated? (infarction)
T - T wave - any abnormal or inverted T waves? NORMALLY INVERTED IN AVR, V1. if inverted in any other then could be ischaemia or ventricular hypertrophy.
physiologically explain these ECG findings
- narrow complex tachy
- broad complex tachy
- complete heart block
- sinus arrhythmia
- extrasystoles
- af
- vf
narrow complex - electrical activation starts in sinoatrial node, atrial muscle or AV node. rate usually >120bpm, p waves may or may not be visible
broad complex - electric starts from ventricles at a rate faster than from sa node, no p waves, >120bpm
complete heart block - atria and ventricles not synchronized and work independently, but both are beating reg due to intrinsic activity. p and QRS completely independent
sinus arrhythmia - normal ECG except affected by resps - this is normal, distance between QRS is shorter during insp
extrasystoles - aka ectopic beats which may originate from atria, AV node or ventricles and basically just come early making it look irregular - if from supraventricular (atria or AV node) then = narrow QRS, if from ventricles = wide QRS
af = totally disorganised atrial electric, no p waves, irregularly irregular, QRS can be narrow
vf = totally chaotic ventricular activity without efficient pump = death without resus - squiggle on sheet
ECG red flags and what they could indicate
> 120bpm <45bpm = ischaemia, hypotension, sepsis
af = valve disease, alcoholism, ischaemia, infection
complete heart block = any heart disease
ST elevation or depression = infarction or ischaemia
abnormal t wave inversion = infarction, ischaemia, PE
wide QRS = any heart disease
what is PASP
pulmonary arteries systolic pressure - on ECHO based on the velocity of the ejection of the pulmonary valve, we can work out how hard the pressure is there - if >40mmhg then there is high pressure there
what happens if something goes wrong with the conduction system
arrhythmia (tachy, brady, sudden death)
what happens if there is a problem with the coronary blood supply
angina
MI
how is angina stable?
when coronary art disease becomes obstructive, this can cause angina
these plaques are stable - strong fibrous cap protects the blood from exposure to the lipid core of the lesion - preventing thrombosis
when seeing someone with chest pain your immediate diagnoses in ur head are
STEMI
angina/unstable
NSTEMI, awaiting trop confirmation
other - PE, aortic dissection, reflux, MSK pain
atrial fib AF causes patho types RF symps assoc ECG ix mx comp
causes
anything that causes atrial stretch - HTN, HF, valve disease, lung disease, obesity, age, hyperthyroid, alc
patho
rapid chaotic atrial firing causes stagnation of blood in atria leads to thrombus formation and risk of embolism - > high risk of stroke
reduction of cardiac output may lead to HF
types
paroxysmal - spont term within 7 days normally <48 hours
recurrent - 2+ episodes
persistent - last longer than 7 days, can degen to permanent
permanent - long standing > 1 year, not successfully terminated by cardioversion
RF age HTN HF CAD valvular DM CKD
symps
none or tiredness/dizziness/ breathlessness, palps.
chest discomfort
or just generally ‘off’
assoc
SVT
ECG absent p oscillating baseline atrial rate - 350-600 vent rate 100-180 irreg irreg
ix ECG +/- 24 hour ambulatory ECG for paroxysmal TFT FBC UE renal func LFT/coag for warfarin imaging - transthoracic echocardiogram
mx
main priority is thromboproph, then sympt improvement with rate or rhythm control
if needed then:
RATE
- first line BB or limiting CCB (diltiazem, verapamil), dual therapy + digoxin or two of: BB, diltiazem, dig
RHYTHM
>48hrs OF AF
anticoag with warfarin 3w or NOAC if high stroke risk (calculate CHADS2-VASc score) before cardioversion
alternative = transoesophageal echo to exclude left atrial appendage thrombus- then can be heparinised and cardioverted immediately.
electrical > pharma for this.
if high risk of cardioversion failure then 4w amiodarone or sotalol prior
post cardioversion - 4 weeks anticoag
<48hrs OF AF
heparinise
if risk of ischaemia - lifelong anticoag
offer transoesophageal electrical cardioversion - consider amiodarone if structural heart disease. if unsuccessful BB or dronedarone or amiodarone (if no HF or LV dysfunction), dont use fleicanide if ischaemic or structural
if drug rx fails - left atrial catheter ablation (if paroxysmal) or pace and ablate (if perm) at AV node - will need anticoag 4 weeks before + during procedure
lifestyle factors - weight loss, diet, reduction of alc
comp
stroke
HF
cardiomyopathy
paroxysmal supraventricular tachycardia def types causes patho course symps mx
def
HR >100bpm
narrow QRS <0.12s unless related to BBB
types atria or SA node: - sinus tachy - AFib - AFlutter - Atrial tachy AV node - junctional: - AV re-entrant tachy AVRT - AV nodal re-entrant tachy AVNRT - sino-atrial re-entrant tachy - lown-ganong-levine syndrome - mahaim-type pre-excitation - also has LBBB morph with right accessory pathway
causes drugs conduction disease (age) surgery aortic endocarditis
patho
circus movement tachycardias with reentry circuit set up
in diastole coronary blood flow increases. As HR increases diastole shortens. Decreased flow to heart with increased ventricular rate
course
onset is sudden
initiated by prem beat
stop abruptly but may recur - hence paroxysmal
symps usually intermittent palps syncope/presyncope fatigue light headed
MANAGEMENT
most dont need mgmt
but if symptomatic or need to prevent comps:
ABCDE
o2 + IV access
whack on monitoring - ECG, BP, sats, record 12 lead
YES adverse features? aka shock, syncope, MI, HF -> DC cardiovert up to 3 times -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours
NO ADVERSE FEATURES:
1. REGULAR
vagal manoeuvres
IV adenosine - 6mg -> 12mg -> 12mg with ECG monitoring (CI in asthmatics, use verapamil instead)
if rhythm restored -> probs re-entry paroxysmal SVT, do another 12 lead in sinus, if recurs give adenosine again
if rhythm not restored -> A flutter - get expert help + BB
IRREG
? AF IVBB or diltiazem, consider IVDig or amiodarone if evidence of HF, if <48 hrs IV amiodarone
regular attacks reduced by secondary prevention - anti-arrythmic drugs (BB, flecainide, amiodarone etc)
usually cured by invasive ablation - requires electrophysiological study
ventricular tachy def of VT patho morphological classification of VT ECG features causes symps mx comps
def
usually reg, broad >0.12 QRS
>3 PVCs in a row at >100bpm
may be sustained >30s or non-sustained
patho
Re-entry, increased myocardial automaticity. Re-entrant circuits often occur in zone of fibrosis or ischaemia surrounding damaged myocardium e.g. post MI
morphological classification
monomorphic - uniform morphology
polymorphic - varying
torsades-de-pointes - variant type of polymorphic VT with cyclic variation of complexes and associated with long QT syndromes - can degen to VF
ECG features AV dissoc fusion + capture beats QRS concordance in chest leads - +VE indicates origin on post ventricular wall (wave moves towards chest leads) bizarre QRS axis RSR complexes in V1 (bad rabbit ear) if starts in left = RBBB if in right = LBBB
causes drugs conduction disease (age) - re-entry commonest surgery aortic endocarditis
symps tiredness dizziness breathlessness sudden death - supraventricular syncope normally haemodynamically unstable requiring immediate help - supra
mx
ABCDE, access + 02 + monitoring (ECG, BP, sats)
immediate DC cardioversion
recurrence - up to 3 shocks
amiodarone 300mg IV over 10-20mins and repeat shock then 900mg over 24 hours if refractory
if irreg/stable - AF with BBB rx as narrow complex, polymorphic VT = magnesium 2g over 10 mins
if reg/stable - VT amiodarone as above, if prev SVT consider adenosine
as this is usually due to damage prevention is needed by regular anti-arrythmic drugs: BB/CBB,
common to require implantable cardioverter defib unless having an acute MI
if drug therapy fails -> electrophysiological study
comps
may degen to VF
causes of HF
previous MI HBP genetic causes drugs (chemo, alc) idiopathic
classification of HF
HF with reduced ejection fraction
preserved Ejection fraction
standard assessment of pump function
transthoracic echocardiogram (USS)
ix of HF
mainstay is transthoracic echocardiography to detect ventricular impairment
newer test for elevated serum B-type Natriuretic peptide
cardiac MR
Describe different devices that can be inserted and what for
single chamber pacemaker - in RA or RV
dual chamber pacemaker - bradyarrhythmia, IN RA/V
implantable cardioverter/defib - treat VT or VF. can also pace bradycardias
cardiac resynchronisaton therapy - mx HF. can also pace bradycardia (CRT-P). has leads into RA + V, AND LV
causes of valve disease
degen RF congenital endocarditis papillary muscle rupture after MI
ix of valve disease
diagnosis - transthoracic echo
transoesophageal better images particularly of mitral
types of valve replacement
metallic prothesis - requires lifelong warfarin, which can only be stopped if bridged with heparin. NOACs not used.
biological (tissue from donor or animal)
pain on walking, relieved by rest - what are the two important ddx
spinal canal stenosis or Intermittent Claudication
- can be differentiated by asking if its worse going downhill = spinal canal stenosis
uphill = intermittent claudication (working harder)
peripheral vascular disease - def classification pres O/E ddx ix mgmt comp
def Narrowing of arteries distal to AoAr most often due to atherosclerosis
classification Fontaine: 1) asymptomatic, 2) intermittent claudication, 3) ischaemic rest pain, 4) critical limb ischaemia (*ischaemic rest pain + ulceration/gangrene) + acute limb ischaemia (sudden decrease in perfusion due to thromboembolism)
rutherford
I - Ischaemic but not threatened - no neuro or muscle tenderness, but delayed cap refill, doppler monophasic
IIa - Ischaemic and threatened but not immediate - +mild sensory and rest pain
IIb - Ischaemic and immediately threatened - severe rest pain, sensorimotor deficit, muscle tenderness, no cap refil, no doppler signals
III - Irreversible ischaemia (Not
salvageable) - severe rest pain, profound sensorimotor, profound pallor with fixed cyanotic skin, no doppler, raised CK, lactate and met acid
pres
Intermittent claudication
Cramping pain in calf, thigh, buttock on walking. Symptoms worse uphill. Relieved by rest. Rest time, claudication distance.
Ischaemic rest pain
Severe unremitting pain in foot, stops from sleeping, relieved by dangling or foot on cold floor
O/E
Absent/reduced femoral pulse (+ popliteal, posterior tibial and dorsalis pedis)
Trophic changes: pale, cold, hairless, skin change
Ulcers, poorly healing wounds, gangrene if diabetes review in 24 hours (amputation)
Buerger’s angle 20 degrees, cap refill prolonged
ddx
Sciatica, spinal stenosis, DVT, entrapment
ix
BP, FBC (anaemia aggravates), ESR (giant cell arteritis), thrombophilia screen, BG, lipids, ECG (CAD), renal function, urine dip
*Doppler ultrasonography (dublex) to calculate ABPI: SBP ankle/SBP arm
Normal = 1
<0.9 = mild PAD, <0.8 = mod, <0.5 = ischaemic rest pain
mgmt
CV RF: smoking, ex (2hrs/week for 3 months), weight, statins, ACEI (*but beware renal artery stenosis), manage DM, manage HTN
Antiplatelet therapy: *clopidogrel +…
best medical treatment targets - <140 systolic, total chol <4, LDL <2, HBa1c <59
Supervised exercise (2hrs/week)
Vasodilator therapy - e.g. naftidrofuryl oxalate
Imaging if considering revascularisation: Duplex USS ± CT angiography
Revascularisation if suitable and attempted CVRF - angioplasty and stenting
CI
Assess by vascular MDT
Manage pain: paracetamol + weak/strong opioid
Imaging: Duplex USS ± contrast enhanced CT angiography
Revascularisation with angioplasty and stenting (percutaneous transluminal angioplasty) - aorto-bifemoral bypass graft, femoro-popliteal bypass graft
?Amputation
comp
*Acute limb ischaemia due to thrombus or embolism
*6 Ps: pale, pulseless, pain, perishingly cold, parasthesia, paralysed
*mottling -> irreversible
Urgent hand-held doppler + urgent angiography:
Requires re-vasc in 4-6 hours with *immediate heparinisation
If embolism = surgical embelectomy (Fogarty balloon emolectomy catheter)
If thrombotic = thrombolysis, angioplasty or bypass
*Find the source of the emboli: ECG, echo, aortic USS
Infection and poor healing
Gangrene
compartment syndrome what isit features diagnosis mgmt post op comps
def is a particular complication that may occur following fractures (or following ischaemia reperfusion injury in vascular patients). It is characterised by raised pressure within a closed anatomical space (fibro-osseous compartments). The raised pressure within the compartment will eventually compromise tissue perfusion resulting in necrosis. The two main fractures carrying this complication include supracondylar fractures and tibial shaft injuries
features
Pain, especially on movement (even passive)
excessive use of breakthrough analgesia should raise suspicion for compartment syndrome
Parasthesiae
Pallor may be present
Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
Paralysis of the muscle group may occur
diagnosis
Is made by measurement of intracompartmental pressure measurements. Pressures in excess of 20mmHg are abnormal and >40mmHg is diagnostic
mgmt
This is essentially prompt and extensive fasciotomies
In the lower limb the deep muscles may be inadequately decompressed by the inexperienced operator when smaller incisions are performed
Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients require aggressive IV fluids
Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to be considered
Death of muscle groups may occur within 4-6 hours
painful leg post bypass surgery ddx
ddx graft occlusion compartment syndrome reperfussion DVT
AAA normal diameter of aorta types pathophys pres ix surveillance mgmt
normal diameter
2cm so AAA >3
growth 1-6mm/year with AAA
types
True aneurysms are an abnormal dilation of an artery due to a weakened vessel wall. By contrast, false aneurysms are external hematomas with a persistent communication to a leaking artery.
causes
atherosclerosis
pres
Mainly asymptomatic: often incidental finding
Pain in back, abdomen, loin or groin *DDx for loin to groin
Pulsatile abdominal swelling
May rupture -> shock
Distal trashing - dusky fingers from dislodged thrombus debris
O/E
Bimanual palpation supra-umbilical - detect 60%>3cm and 80>5cm
Abdominal bruit
Retroperitoneal haemorrhage - Grey Turner’s sign = flank bruising
ix
FBC, clotting, renal, liver, crossmatch, ESR/CRP
ECG, CXR
*USS for initial assessment
CT for more anatomical detail, evidence of mural thrombus - *crescent sign - indicates blood within thrombus - imminent rupture
MRI angiography
mgmt
Small = < 5.5cm, large = >5.5cm
Regular USS monitoring
3-4.5cm = yearly, 4.5-5.5cm = 3 monthly, 5.5cm or larger - consider surgery
Medical mgmt: smoking, HTN, statin, antipt, low dose aspirin
Inform DVLA at *over 6cm
Elective surgical repair if >5.5cm or rapid expansion >1cm/year or symptomatic:
Open EndoVascularAR
screening
offer at 65 if USS neg - rules out AAA for life
DVT
pathophys
ix
mgmt
patho
virchows triad - stasis, hypercoagulability, endothelial damage
ix two-level wells score: active cancer <6m immobilisation of leg bedridden >3 days or maj surg<12w localised tenderness entire leg swollen calf swelling >3cm to other side pitting odema on just sympt leg collateral superficial veins prev DVT alt diag as least as likely - -2
DVT likely = 2+
unlikely = 1 point or less
mgmt
DVT likely => proximal leg USS <4hrs - +ve anticoag
-ve then d-dimer
if not <4hrs then d-dimer and anticoag in meantime
anticoag - apixaban (DOAC) for at least 3 months if provoked, if unprovoked 6 m
use of Hand Held Doppler
arterial signal
ABPI
venous reflux
name 4 vascular emergencies
acute ischaemia
diabetic foot sepsis
leaking AAA
bleeding
signs of critical limb ischaemia
pain hair loss nail atrophy ulcers gangrene
what is the additive in these blood bottles:
gold
green (dark or light)
purple
gold - clot activator and serum separating
green - heparin
purple - EDTA (anticoag)
what is the approx conc of intracellular and extracellular levels of potassium
150mmol/l intra
4mmol/L extra
what is the electrical properties of excitable cells dependant on
potassium
if you have abnormalities in potassium conc what can you expect (cellular level)
cell hyperpolarisation
increased duration of action potential or refractory period
how does potassium move in and out of cells
Na/K-ATPase channel - active transport that requires energy for it to transport (because they move against their conc gradients)
how does B-agonists do to the bodys levels of potassium?
causes hypokalaemia
by stimulation of Na-K-ATPase channels in tissues such as skeletal muscle
where does angiotensin 2 work on the nephron
PCT
on the Na-HCO3 channel
where does aldosterone work on the nephron
late distal tubule + collecting duct at the Na-K-ATPase channels
where is potassium reabsorbed from in the nephron
thick ascending limb on loop of henle
put back in via the Na-K-ATPase channel on the collecting duct
action of diuretics on the nephron - where and how they work
(exports as in out of tubule to body)
carbonic anhydrase inhibitor - acetazolamide = PCT, inhibits exports of Na/HCO3 channel
loop diuretics - furose, bumetanide, torsemide, ethacrynic acid = thick ascending limb of loop of henle, inhibits Na, 2Cl, K export channel
thiazide diuretics - hydrochlorothiazide, chlorothiazide = DCT, inhibits Na, Cl exports
ADH - increases H20 absorption at late DCT/collecting duct
k+ sparing - spironolactone, eplerenone = late DCT/collecting duct, block the action of a hormone called aldosterone and this causes the kidney to pass out more fluid and keep potassium.
where does the kidney detect changes in blood pressure
juxtaglomerular cells on the afferent arteriole that activates B2 receptors causing release of renin -> RAAS system
explain the RAAS
decrease BP = low renal perfusion - juxtaglomerular appartus releases renin - this increases conversion of angiotensinogen to angiotensin 1.
this goes to lungs to find ACE and changes to angiotension 2.
this goes to adrenals which converts steroid precursors to aldosterone.
aldosterone = nacl reabsorption + k+ excretion and h20 retention.
effects of angiotensin 2
increases sympathetic activity
nacl reabsorption + k+ excretion and h20 retention.
arteriolar vasoconstriction
pit gland post lobe - ADH secretion - collecting duct - h20 absorption
what hormones/body states are responsible for driving k+ into cells
insulin + catecholamines
acidaemia - k+ + h+ are exchanged at tissues and result in hyperkalamia. hydrogen and potassium ions compete with each other for exchange with sodium ions across cell membranes and in the distal tubule.
where do you find angiotensinogen
liver
how can you reduce the effects of angiotensin 2
Angiotensin receptor blockers (ARBs), also known as angiotensin II receptor antagonists, are used to treat high blood pressure and heart failure. They are also used for chronic kidney disease and prescribed following a heart attack. They include valsartan, losartan and candesartan.
hyperkalaemia ECG changes
tenting T waves
flattening/loss of p waves
broad QRS complex
sine wave appearance - progressively widened QRS eventually merges with T wave, forming sine wave pattern - VF or asystole follows.
can cause eventually heart blocks
hyperkalaemia severity causes pseudohyperkalaemia pres ix mgmt
severity
mild - 5.5-5.9
mod 6-6.4
severe >6.5
causes acute kidney injury drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin (through inhibition of aldosterone) metabolic acidosis eg DKA Addison's disease rhabdomyolysis, burns, trauma massive blood transfusion beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment digoxin
pseudohyperkalaemia
tourniquet + clenched fist
pres non specific weakness fatigue flaccid paralysis depressed tendon reflexes palps chest pain
ix U/E check for tox eg dig ABG - met acid ECG - no p wave, broad QRS, slurred s wave, peaked T wave
mgmt
ABCDE + 12 lead ECG
find cause - stop/treat
emergency correction =
1. stabilise cardiac membrane - IV calcium gluconate (this does NOT lower pot) 10 10 10 - 10ml 10% every 10 min
2. short-term shift pot from extra to intra - insulin/dex infusion, neb salbutamol
3. removal of pot from body - calcium resonium (enema most effective), loop diuretics, dialysis (haemofiltration/haemodialysis should be considered for patients with AKI with persistent hyperkalaemia)
ECG changes in hypokalaemia
reduction in T wave amplitude
depression of ST segment
U waves - small positive deflection after the T-wave in V2/3
prolong PR
U have no Pot and no T, but a long PR and a long QT
hypokalaemia classification causes features ix mgmt comp dig relationship to k
classification
mild 3.1-3.5
mod 3.5-3
severe <3
causes
alkalosis - vomiting, thiazide + loop diuretics, cushings, conns
acidosis - dirrhoea, renal tubular acidosis, acetazolamide, partially treated diabetic ketoacidosis
inadequate intake - TPN, IV
features mild - asymp <3 = muscle weakness/pain, constipation <2.5 = neuromuscular probs, severe ascending paralysis and weakness -> resp failure, ileus + hypotonia, parasthesia + tetany
ix u+e bicarc glucose serum mag ECG - to detect dig tox
mgmt
pot replacement - mod/low risk = sandok,
IV replacement NEVER BOLUS, NEVER >10MMOL/HR
with cardiac monitoring + 1-3 hourly bloods
magnesium deficiency - always treat mag deficiency first!!
comp
cardiac arrhythmia + sudden death
dig
Digoxin and K inhibit each others binding to Na/K ATPase
Hyperkalaemia reduces digoxin activity, hypokalaemia increases activity
anatomy of electrical conduction of the heart
SN node atrium AV node bundle of His L and R bundle branches purkinje fibres
what is a quick way of working out HR on an ECG thats in reg rhythm
R-R interval large sq 1 = 300bpm 2 = 150 bpm 3 = 100bpm 4 = 75pm 5 = 60pm 6 = 50pm
what does the ST segment represent
ventricular contraction
what can a prolonged QT interval lead to?
ventricular tachycardia
if R + S are: 1. predom up 2. predom down 3. even in size what does that mean
- depolarisation is moving towards that lead
- depolarisation is moving away
- depolarisation is perpendicular to that lead
what can axis deviation mean
strain on the R or L of the heart causing increase work and size of the muscle on that side that is causing a greater electrical effect on that side skewing the electrical axis.
what do the individual chest leads look at
v1/2 - RV
V3/4 septum
5/6 - LV
how to report an ECG to a senior
- rhythm
- conduction intervals
- cardiac axis
- description of QRS complexes
- description of ST segments and T waves
followed by ur interpretation:
normal or abnormal
then the ?underlying pathology that would cause this
bradycardia def causes symps mgmt
def
bradycardia + AV block
<60bpm
sinus brady - every p wave followed by a QRS + <60bpm
causes
physiological - athletes, young due to high resting vagal tone
patho - acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP
pres syncope fatigue dizziness ischaemic chest pain palps
mgmt
if rate >40bpm but asymp dont treat, but look for cause and maybe change drugs
if <40bpm or symp:
IV atropine 500mcg (in emergency) - anticholinergic i.e muscarinic antagonist, reduces vagal tone
not worked? give more up to 6 doses
try noradenaline
temp pacing wire - transcutaneous cardiac pacing
long term - permanent implantable pacemaker - specialist review
sick sinus syndrome def causes ECG assoc mgmt
def result of dysfunction of SA node with impairment of ability to generate impulse
causes
idiopathic fibrosis of node - assoc with ischaemia + dig tox
ECG
sinus brady
sinoatrial block - transient failure of impulse conduction to atrial myocardium, pause between p waves
sinoatrial arrest - prolonged pause without p wave activity, unrelated to PP interval
assoc
escape rhythms - spont activity from subsidiary pacemaker located in atria, AV junc or ventricles (junct - normal QRS 40-60bpm, ventricular - broad complex slow 15-40bpm)
mgmt
tachy-brady syndrome or AF
treat if symp - permanent atrial or dual chamber pacemaker
if with tachy + dig or verapamil (anti-arrhythmic)
s/e of atropine
inhibits parasymp so pupil dilation
urinary retention
dry eyes
constipation
AV block
def
causes
types + their pres/ECG + mgmt
AV conduction may be delayed, intermittently blocked or completely blocked. abnormal conduction of AV node or bundle of His
causes MI/ischaemia (inferior) infection - lyme disease immunological (SLE) myocarditis endocarditis degen of his-purkinje drugs - dig, BB, CCB
types 1ST DEGREE BLOCK delay of atrial impulse to ventricles - PR >0.2s constant - every P followed by QRS pres - benign
2ND DEGREE BLOCK
intermittent failure of conduction from atria to ventricles. some P are not followed by QRS.
MOBITZ TYPE 1 aka Wenkebach. failure at AV node level. PR progressively lengthens then is blocked.
pres - usually asymp, mgmt if symptomatic or inferior MI cause
MOBITZ TYPE 2 - intermittent failure of P wave conduction and loss of QRS. failure at bundle branch therefore wide QRS. PR constant but prolonged. 2:1 or 3:1 block.
risk of asystole
if symp pacing required
atropine useless as past AV node
2:1 BLOCK - difficult to tell whether its mobitz 1 or 2. but can be caused by dig tox or ischaemia
3RD DEGREE BLOCK
complete failure of conduction of atria to ventricles normally caused by myocardial fibrosis
- independent P and QRS waves: AV dissociation.
- if block in or above HIS (nodal) - QRS narrow rate id 45-60
- if block in or below - wide slow QRS <45
mgmt stable - observe unstable or risk of asystole - mob type 2, complete HB or prev asystole: - atropine 500mcg IV repeat up to 6 times for response - try noradrenaline next - transcutaneous cardiac pacing
RBBB
assoc conds
patho
ECG
ASSOC conds mainly pathological Rheumatic heart disease RVH - could be due to cor pulmonale IHD - aka MI myocarditis cardiomyopathy degen disease of conduction system PE
patho
depolarisation of RV delayed
LV depol normal therefore first part of QRS normal
spread depol from L to R through non-specialised tissue
ECG MarroW - M in V1 and W in V6 QRS >0.12s secondary R wave in V1/2/3 RSR deep wide slurred S wave in 1, V5/6 T wave inversion in V1/2
LBBB
assoc conds
blood supply
ECG
assoc conds coronary art disease HTN heart disease dilated cardiomyopathy anterior infarction
blood supply
LAD + right coronary art therefore if LBBB - extensive disease
ECG WilliaM - wide QRS >0.12s absent Q in V5/6 broad R in I, V5/6 deep S in V1,2 assoc LAD
Treating bradycardia
ix
mgmt
ix
12 lead ECG
Ix for electrolyte imbalance
UE, glucose, Ca, Mg, TFT, toxicology
mgmt
If symptomatic (syncope, hypotension, heart failure) or rate <40:
Resus, IV access
FBC, UE, glucose, Ca, Cr, cardiac enzymes, TFT, digoxin level
Treat cause: correct electrolytes, stop negative chronotropes
Treat bradycardia:
IV atropine 0.5mg (may repeat up to 3mg)
Poor response - transcutaneous pacing
May also try glycopyrrolate (antimuscarinic), glucagon (if due to BB or CCB)
Temporary or permanent pacing (esp @heart block, sick sinus)
types of broad complex tachycardias
classic patient
signs
ventricular tachy
regular - monomorphic, right venticular outflow tract, fascicular
irreg - torsades de points, polymorphic ventricular tachy
supraventricular
with aberrant conduction or ventricular pre-excitation any SVT may present as broad
aberrant conduction - usually manifests as LBBB or RBBB
WPW
AF with AV re-entrance
patient
>35, hist of IHD or CHF
signs
AV dissociation: cannon waves in JVP, variable intensity first heart sound
sinus tachy - SVT def causes ECG ix mgmt
def every P followed by QRS, >100bpm
causes physiological - exertion, anxiety, pain patho - fever, anaemia, hypovolaemia endocrine - thyrotoxicosis, phaemochromocytosis pharma - adrenaline, albs, alc, caffeine
ECG
every P followed by QRS
rate 100-200
ix 12 lead ECG cardiac enzymes RBC TFT
mgmt
acute - haem stable (ie not hypotensive)
- vagal manoeuvres: carotid massage, vasalva, facial immersion in cold water
ongoing
- exlude BB or non-dihydropyridine CCB (diltiazem, verapamil)
ectopic atrial tachycardia SVT source atrial rate ECG types
source
ectopic in atrial muscle
rate - 150-250bpm
ECG
ectopic unifocal p waves usually precede normal looking QRS complexes, unless aberration present
usually <250bpm
abnormal p wave morphology - inverted p waves in inferior leads
rate 150-250
variable ventricular rate but reg
may have varying degrees of AV block
types benign - elderly 80-140bpm incessant ectopic multifocal - COPD, varying p wave morph atrial tachycardia with block - dig tox (baso a fast heart block)
ectopic atrial rhythm is similar but rate <100 bpm
AF def/types assocs patho ECG mgmt
def/types classified according to duration: - first ep - recurrent (>2 eps) - paroxysmal (lasting <7days) - persistent (>7 days) - long standing persistent (>1 year) - permanent (>1 year if rhythm control not successful or attempted)
asssocs most forms of heart disease: - CAD - HTN - valvular - congenital - cardiomyopathy some metabolic - thyrotoxicosis and toxins eg alc
patho
mechanism unknown
disorganised atrial electrical and contractile activity
ECG
absence of P-waves
irregularly irregular activation of ventricles
fine fibrillatory waves visible in ECG baseline
‘ashman phenomenon’ - aberrantly conducted ventricular beats usually with RBBB morphology
mx
high risk of thromboembolism -> CHA2DS2-VASc score to figure out if to anticoag
rate vs rhythm control with drugs
DC cardioversion +/or ablation therapy
atrial flutter what is it classification causes ECG ix mgmt
what is it
regular narrow complex tachycardia
caused by re-entry circuit in RA
classification TYPICAL (type 1) - involving the IVC and tricuspid isthmus with anti-clockwise re-entry producing inverted/neg flutter waves in leads I, II, aVF and positive waves in V1. ATYPICAL (type 2) - atrial rate is higher and rhythm more unstable. less amenable to ablation than type 1.
causes
similar to AF
most common - CAD, HTN, hyperthryoid, obesity, alc, COPD
ECG
saw tooth flutter waves visible on ECG rate of 300bpm atria (200-400). ventricular rate determined by degree of AV block, 2:1 the commonest + 4:1. if 1:1 can happen via accessory pathway (WPW), progresses to VF and is medical emergency.
no p waves
therefore 2:1 atrial flutter should always be suspected with someone who presents with 150bpm + narrow complex tachy
ix ECG +/- 24 hour ambulatory ECG for paroxysmal TFT FBC UE renal funct LFT/coag for warf imaging - echo for underlying cardiac function
mgmt
similar to fibrillation but more sensitive to cardioversion
ventricular rate slowed with digoxin, BB or CBB
DC cardioversion to convert to SR
definitive therapy - radiofrequency ablation to tricuspif isthmus
anticoag
premature atrial complexes (PACs)
def
ECG
def
extra beats that originate outside the sinus node
from ectopic atrial pacemaker
appear interspersed throughout an underlying rhythm
can be single or repetitive
ECG
ectopic premature P wave
always incomplete pause after a PAC, owing to reset the sinus node
the ectopic p wave normally generates a QRS complex
ashman beat
LONG SHORT WEIRD
long R-R interval followed by short R-R interval then a disrupted QRS with RBBB morphology (M)
Premature junctional complexes
def
ECG
def
simiar to PAC but less frequent
ectopic beat that originates in atrio-ventricular node + His bundle
p wave is negative
compensatory interval is shorter than PAC
simultaneous capture of the atria (retrograde) and ventricles (anterograde)
ECG
retrograde P wave before or after QRS (often hidden) in inferior leads
usually short PR interval
mutlifocal atrial tachycardia
def
discrete multifocal p waves with differing morphologies
several ectopics happening in atria firing off currents
100-250bpm
varying PR intervals followed by normal QRS complexes unless aberration present
ventricular response is irregularly irregular
can be confused with AF - but you do have p waves so cant be AF
if rate <100bpm its called multifocal atrial rhythm
AV nodal re-entrant tachycardia AVNRT epi onset patho ECG mgmt
EPI
most common
onset
late teens or early 20s
abrupt + offset following PAC
patho
- Two functionally and anatomically different pathways in AV node with common path in lower AV node and bundle of His. One path fast with long refractory, one slow with quick refractory.
- In sinus, travels down fast and depolarises ventricles, also travels down slow but common path is still refractory
- Slow pathway recovers first, AVNRT initiated if premature atrial beat at critical moment when fast pathway refractory.
Impulse travels down slow then
retrogradely up fast creating re-entry circus
motion
pres sudden onset palps SOB syncope neck pulsation
ECG hr 150-250bpm reg rhythm narrow QRS p wave is retrograde but may not be visible in II, III, AVF (inferior leads)
mgmt
terminated by vagal manoeuvres and AV nodal blocking drugs eg adenosine (short acting and works on AV node) , proph - BB/CCB + adeno
curative - radiofrequency ablation
FULL MANAGEMENT
most dont need mgmt
but if symptomatic or need to prevent comps:
ABCDE
o2 + IV access
whack on monitoring - ECG, BP, sats, record 12 lead
YES adverse features? aka shock, syncope, MI, HF -> DC cardiovert up to 3 times -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours
NO ADVERSE FEATURES:
1. REGULAR
vagal manoeuvres
IV adenosine - 6mg -> 12mg -> 12mg with ECG monitoring (CI in asthmatics, use verapamil instead)
regular attacks reduced by secondary prevention - anti-arrythmic drugs (BB, flecainide, amiodarone etc)
usually cured by invasive ablation - requires electrophysiological study
AV reentrant tachycardia syndrome AVRT def syndrome + classification ECG types of conduction in syndrome worries in syndrome mgmt
def re-entry circuit involves AV node and an extra-nodal bypass pathway
most common extra-nodal conduction pathway is the accessory pathway known as Bundle of Kent in the WPW syndrome - this is a congenital atrio-ventricular bypass tract which can exist in a variety of locations and in some patients there are multiple pathways.
can conduct in both directions but rare
this can cause early activation of ventricles = pre-excitation
WPW = risk of sudden death
classification -
Type A - less common, accessory pathway in left = positive delta-wave in all precordial leads, dominant R wave in V1
Type B = much more common, pathway in right side of heart. neg delta wave in leads V1/2, no dom R wave in V1
assoc with LAD
ECG short PR interval <0.12 delta-wave with slurring of R wave wide QRS >0.11 repolarisation is abnormal causing inverted T wave
types of conduction ORTHODROMIC - common, antegrade conduction via normal pathway, retrograde conduction via accessory pathway QRS can be normal p-waves buried in QRS or retrograde ST depression + T dep common 200-300bpm ANTIDROMIC - less common, antegrade conduction via accessory pathway, features of pre-excitation, wise QRS . p waves buried or retrograde HR 200-300bpm
worries
AF can occur in WPW and sometimes flutter - the accessory pahway can allow for rapid conduction, bypassing AV node = high ventricular rates -> VT or VF
wide QRS complex owing to abnormal ventricular depolarisation via accessory pathway
irregular rhythm
potentially lifethreatening
mgmt
definitive = radiofrequency ablation of accessory pathway
med =
- sotalol (should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation)
- amiodarone
- flecainide
junctional rhythms and tachycardias def: junctional escape beats junctional escape rhythm accelerated junctional rhythm non-paroxysmal junctional tachy
junctional escape beats - av node takes over from SA node as pacemaker if a problem, creating a 40-60bpm
junctional escape rhythms - defined as 3 or more junctional escape beats in succession. AV dissociaton or retrograde atrial capture. can occur normally in athletes or in sinus node disease or BB
accelerated junctional rhythms - active junctional pacemaker firing at rate of 60-99bpm - result of ischaemia, inflam, drugs and some electrolyte disturbances. retrograde p waves in ST segment.
QRS appears normal.
non-paroxysmal junctional tachycardia
accelerated junctional rhythm but with a rate of >/=100bpm
premature ventricular complexes def ECG causes pres differentiating from PAC
def
arise as ectopic impulses from ventricular myocardium both RV + LV
can be one off or more
if frequent = >10 per hour on 24 hr ECG monitoring
ECG
wide QRS
t wave in opposite direction to the R wave with a full compensatory pause
if from RV = LBBB QRS pattern, LV = RBBB pattern
causes
common in fit healthy indi but can be assoc with:
- underlying heart disease (HTN, CAD, valvular, CM, congenital)
- drugs - antidep, aminophylline, dig, amphetamines, anaesthetic agents, cocaine, caffeine, alc
- infection
-stress
- electrolyte disturbances
pres can be asymp palps sensation of missed beats heart thumps dizziness dyspnoea chest pain syncope - rare
differentiating from PAC - this one has same space between two R waves around etopic as before when in sinus = complete rest. in PAC these distances will be different
abberant ventricular conduction
def
causes
ECG
temp alteration of QRS morphology under conditions where a normal QRS would be expected. can occur with sinus beats or ectopics and sustained arrhythmias.
causes
ashman phenomenon is one cause as well as tachy/brady or cos of an accessory pathway
ECG
QRS complex = RBBB morphology
benign sustained ventricular arrhythmias - accelerated idioventricular rhythm def
ECG
causes
course
def
ectopic ventricular pacemaker exceeds sinus rate leading to independent ventricular rhythm
AV dissociation is present but fusion and sinus capture beats are often present
ECG
reg broad QRS complexes >120ms
rate 50-99bpm
= 3 beats in a row qualifies as this
causes common after reperfusion by thrombolysis or PPCI in STEM, dog tox electrolyte disturbance high vagal tone in athletes
course
usually benign + self-limiting
benign sustained ventricular arrhythmias - ventricular/idioventricular escape
def
ECG
causes
def
in normal heart there is a hierachy of pacemaker tissues with different intrinsic depolarisation rates.
usually subsidary pacemakers are suppressed from above ie by the SA node in NSR
if sequence interrupted a lower pacemaker takes over
in idioventricular escape the block occurs above the ventricles usually in the AVN but mybe higher
ECG
broad QRS >0.12
rate 20-50bpm
causes 3rd degree AV block sinus arrest SA block hyperkalaemia AV nodal blocking drugs eg BB, CCB, dig
benign sustained ventricular arrhythmias - ventricular parasystole
def
assoc
def arise from protected ventricular ectopic focus that fires at a fixed rate independent of the basic rhythm, usually sinus = parallel rhythm with varying coupling intervals with an underlying rhythm
assoc
structural heart disease
super rare
what does precordial leads mean
chest leads
what is positive /neg concordance
all the waves go up from the base line
neg all go down from baseline
define fusion and capture beats
Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration. Fusion beats — occur when a sinus and ventricular beat coincides to produce a hybrid complex.
syndromes assoc with ventricular tachys
accquired heart disease eg CAD congential long QT Brugada syndrome Hypertrophic cardiomyopathy dilated cardiomyopathy catecholamine polymorphic ventricular tachycardia syndrome drug tox - tricyclic antidep, antiarrhythmics electrolyte disturbance espesh K +
ventricular fibrillation VF def rf causes ECG mgmt survival
def
disorganised and chaotic heart rhythm in which effective pumping action of the ventricles ceases causing ‘cardiac arrest’
fatal
rf
CAD
acute MI
chronic infarction scar
causes VT AF antiarrhythmic drugs can be idiopathic sudden arrhythmic death syndrome - affects 500 people p.a in uk electrocution drowning
ECG chaotic - varying amplitudes no identifiable P, QRS, T rate 150-500 amplitude decreases with duration: coarse AF to fine AF
mgmt
acute: immediate CPR
rapid electrical defib ideally with biphasic modality
long term - BB and implantable cardioverter defibrillator
survival
out of hosp <10%
in hosp 24%
sino-atrial exit block
patho
types
patho
sinus node has two types of cells, a core of pacemaker (P) cells which generate the impulse and
an outer layer of transitional (T) cells which transmit the impulses to the RA. In S-A Exit Block the P
cells continue to fire but there is malfunction/failure of transmission by the T cells
types
1st
2nd - types I + II (only one that can be reliably diagnosed from ECG)
2 TYPE I - has wenckebach phenomenon of progressive worsening conduction - shortening of PP interval until P wave dropped. irreg rhythm. the P-P pause < sum of two preceding P-P before pause. P-P after pause is greater than before.
2 TYPE II - dropped p waves at reg intervals. pause is approx 2x basic p-p, assuming reg rhythm
3rd - complete absence of p waves. rhythm maintained by junctional escape - if not complete pause which may be difficult to distinguish or progress to sinus arrest -> asystole
when would you consider rhythm control before rate control in AF
if the patient had coexistent heart failure first onset AF or obvious reversible cause younger than 65 symptomatic
CHA2DS2VASc
decide whether to anticoag in AF
congestive heart failure +1 HTN (or rx) +1 age >/= 75 +2, 65-74 +1 diabetes +1 prior stroke or TIA +2 vascular disease - including ischaemic heart disease + peripheral +1 sex - f +1
0 = no treatment 1 = males consider anticoag, female no treatment 2+ = anticoag
if chads vasc says no anticoag ensure a transthoracic echo has been done to exclude valvular heart disease which with AF is abso indication for anticoag
offer choice of warfarin or NOAC - always do a HASBLED risk assessment for warfarin before prescribing
HASBLED
risks of starting someone on warfarin or not
HTN - uncontrolled systolic >160 +1
Abnormal renal function (dialysis or cr >200) OR abnormal liver function (cirrhosis, bilirubin >2 times normal, AST/ALT/ALP >3 x normal) +1 each for liver or renal
Stroke hist
Bleeding hist
Liable INR (time in therapeutic range <60%)
elderly >65 years
Drugs predisposing to bleeding (antiplatelets, NSAIDs) or alc use (>8 drinks/week) +1 for each
> /= 3 indicates high risk of bleeding
what makes you consider not warfarinising patients
history of falls
old age
alc excess
hist of bleeds
warfarin INR target
if poor control…
2-3 (non-valv)
prosthetic valves, post MI - 2.5-3.5
switch to NOAC
things that can cause long QT
congen - jervell-lange nielsen (abnormal pot channel)
romano-ward syndrome
drugs - amiodarone, sotalol, class 1a antiarrhythmic drugs, tricyclic antidepressants, fluoxetine, chloroquine, terfenadine, erythromycin
other - electrolyte (hypo cal/kal/magn), acute MI, myocarditis, hypothermia, subarac haem
fascicular tachycardia
patho
ECG
patho
ventricular + broad
origin = posterior fascicle. produces relatively short QRS (0.12-0.14)
ECG
QRS = RBBB + LAD
RV outflow tract
patho
ECG
mx
patho
ventricular + broad
spreads inferiorly
ECG
LBBB + RAD
mx
BB or CBB
broad complex of supraventricular origin
types
differentiating from ventricular tachy + SVT with BBB
danger of misdiagnosis
types
atrial tachy with abberant conduction - broad complex tachy with L or R BBB
WPW if antidromic (travels the opposite way up nerve)
antidromic AV re-entrant tachy
AF with accessory pathway
differentiating
If RBBB ventricular origin if QRS > 0.14s, axis deviation, concordance all deflections positive
If LBBB ventricular origin if QRS > 0.16s, axis deviation, concordance all deflections negative
CHECK PREV ECG, if pre-existing BBB suspect SVT
danger of misdiagnosis
- safest to treat broad complex as ventricular tachycardia
- giving verapamil to pt with VT may cause hypotension, acceleration and death
- could use adenosine to temp block conduction through AV node to find out origin
cardiac arrest arrhythmias
shockable - VF, pulseless VT
nonshockable - asystole, PEA (pulseless electrical activity)
brugada syndrome
what is it
ECG
mgmt
what is it
Genetically inherited condition characterised by abnormal ECG and increased risk of sudden death. Autosomal dominant. Sodium channels
ECG Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T (Brugada sign) \+ Documented VF or PVT Fam Hx sudden death <45 Coved ECG
mgmt
ICD implantable cardioverter defibrillator
PE
ECG
*Sinus tachycardia - main finding
S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%
Assoc RBBB
J wave
Late delta wave, positive deflection at junction of QRS and ST segment, associated with hypothemia
drugs affecting the cardiac action potential class 1-4
class 1 - acts on section 0 of action potential Na channel blocker 1a = moderate: quinidine, procainamide 1b = weak: lidocaine, phenytoin 1c = strong: flecainide, proafenone
class 2 - acts on section 4 BB - propanolol, metoprolol
class 3 - acts on section 3 K+ channel blocker amiodarone, sotalol
class 4 - acts on section 2 ca2+ channel blocker verapamil + diltiazem
drugs affecting AV node
adenosine dig diltiazem verapamil fleicanide
amiodarone indication action adverse effects CI interacts precribing
indication For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work
action
Blockade Na/K/Ca channels, antagonist alpha and beta adrenergic receptors which reduces automaticity, slows conduction and increases refractory period including in AV node (therefore reduces vent rate in AF and AFl)
adverse effects
Hypotension during IV infusion. Chronic use lungs (pneumonitis), heart (AV block), liver (hepatitis), skin (grey discolouration), *thyroid (long half life)
Amiodarone iodine rich and very similar levothyroxine. Can cause hypothyroidism
CI
Severe hypotension, heart block, thyroid disease
interactions
Increases plasma conc of NDHP-CCB and digoxin therefore these should be halved
prescribing
Always requires senior unless in cardiac arrest (after third shock) - give 300mg bolus
adenosine indication action important prescribing
indication
First line diagnostic and therapeutic in SVT (inc junc)
action
Adenosine receptor agonist on cell surface. In heart reduces automaticity and increases refractoriness -> slows sinus rate, slows conduction and increases AV node refractoriness (breaks re-entry circuit) only works if circuit involves AV node.
Blocks conduction to ventricles allowing closer inspection of atrial rhythm
Very short duration - half life 10s
important
Blocks SA and AV node - causes bradycardia and asystole - doom feeling
May induce bronchospasm in asthma or COPD
prescribing
Always IV, must be in once-only
6mg, if ineffective may give 12mg, must always monitor with continuous ECG
digoxin aka indication mech important SE warnings important interactions prescribing monitoring tox symps levels ECG
aka
cardiac glycoside
indication
Reduce ventricular rate (AF, AFl) - after CCB or BB
Severe heart failure - 3rd line
action Negatively chronotropic (HR), positively inotropic (contractility). In AF indirect path increases vagal tone (PSNS - lost in exercise). Reduces conduction at AV node. In HF has direct effect on myocytes - inhibits Na/K pumps causing increased intracellular Na. This means Ca accumulates in cell increasing contractile force (Na/Ca exchange)
important SE
Digoxin toxicity - arrhythmias, low therapeutic index (margin therapeutic to toxic)
Bradycardia, GI upset, visual disturbance (blurred/yellow), headache, nausea
*Gynaecomastia
warnings
CI at second degree heart block. Reduced dose in renal failure. Increased risk of toxicity in *hypokalaemia, hypomagnaesaemia, hypercalcaemia
Digoxin competes potassium at Na/K pump. When serum K low competition is reduced and effect increased
important interactions
Loop + thiazide diuretics cause hypokalaemia - toxicity
Amiodarone, CCB, spironolactone all increase plasma digoxin - toxicity
prescribing
Loading dose in AF/Afl - 15mcg/kg lean body mass orally once daily
In elderly give in divided dose
If no effect give additional 5mcg/kg
Calculating maintenance
Fraction of loading dose adjusted for renal function
100=⅓, 50 = ¼, 25 = ⅕, 10 = ⅙, 0 = 1/7
HF - no loading dose - give 62.5-125mcg PO OD
Can give IV - only if slowly
monitoring Monitor symptoms (or vent rate) + ECG + renal dysfunction + hypokalaemia
tox symps
Nausea, vomiting, diarrhoea, dyspnoea, confusion, dizziness, headache, blurred vision
levels
Plasma concentration digoxin
Target 1.0-1.5nmol/l
Above 2.0nmol/l suggests toxicity
ECG
ST-segment depression - reverse tick sign
CCB eg + usefulness action SE SI prescribing
eg + usefulness
Verapamil (most cardio-selective) + diltiazem (non-dihydropyridine) + amlodipine (dihydropyridine)
action
Rate control in SVT inc AF +AFl
Decrease Ca entry to vascular and cardiac cells induces relaxation + vasodilation in arterial smooth muscle + myocardial contraction in heart.
Suppress cardiac conduction particularly over AV node
Reduced rate, contractility and afterload decreases oxygen demand preventing angina
SE
Ankle swelling, flushing, headache - dihydropyridine e.g. amlodipine
Verapamil - constipation, bradycardia, heart block
Diltiazem (mixed)
CI
Don’t prescribe with BB - both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole
prescribing
HF, bradycardia + asystole
For acute SVT verapamil may be given IV *the only one IV
BB indication action SE CI
indication First line IHD reduce angina CHF improve prognosis AF reduce rate and maintain sinus rhythm SVT to restore sinus rhythm
action
B1 in heart, B2 in smooth muscle blood vessels and airways
Via B1 reduce force and speed of conduction in heart - reduces cardiac work and oxygen demand and increase myocardial perfusion
Prolong refractory period of AV node
Lower BP by reducing renin secretion
SE
fatigue, cold extremities, headache, impotence
CI
Asthma - B2 blockade causes bronchospasm, usually safe in COPD
Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)
Don’t use with NDHPCCB
innervation to ventricles
sympathetic only
innervation to SA/AV node
para + symp components
what is cardiac output
depends on
equation
volume of blood ejected from LV per min
preload, contractility, HR, afterload
SV X HR
mean arterial pressure equation
systemic vascular resistance x CO
starlings law
Preload or degree of stretch is critical factor for stroke volume.
Increased EDV (end-diastolic volume) leads to increased myocardial stretch
Increased myocardial stretch leads to increased contractility and increased stroke volume decreasing end systolic volume
This implies in blood loss - reduce EDV = reduced CO
*preload is EDV, afterload is ventricular pressure at end of systole
where to listen for murmurs
APTM - all prostitutes take money
A - aortic rse 2nd
P - pulmonary lse 2nd
T - tricuspid - rse 4th
M - mitral midclav 5th
murmurs grades
levines scale
Grade 1 Heard by an expert in optimum conditions
Grade 2 Heard by a non-expert in optimum conditions
Grade 3 Easily heard, no thrill
Grade 4 Loud murmur, palpable thrill
Grade 5 Very loud murmur, often heard over a wide area, palpable thrill
Grade 6 Extremely loud, heard without a stethoscope
Heart Sounds
S1 - closure mitral and tricuspid (M1 + T1)
S2 - closure aortic and pulmonary (A2 + P2) - might split on deep inspiration - delayed P2
delayed P2 causes
pulm HTN/ Pulm stenosis
3rd heart sound causes
HF - sounds like galloping horse
when would you hear a:
systolic
diastolic murmur
systolic - between S1 + 2 (may be innocent in children and preg)
diastole - always patho, between S2+1
mitral murmurs
where heard
MR
MS
@apex + radiate to axilla, heard best in left lateral position
MR
Pansystolic - burrrr
MS
Loud opening snap S1 and mid-diastolic murmur - lub de-durrrr
tricuspid murmurs
where
TS
TR
where
Uncommon, timing is as for mitral murmurs @lower right sternal
TS
Pre systolic May occur in RVH, marked wave on JVP
TR
Pansystolic Does not radiate to axilla
pulm murmurs where
PS
PR
L2IS
PS
Crescendo-decrescendo systolic (louder then softer).disappear on inspiration
PR Early diastolic (Graham Steel due to pul HTN due to MS)
aortic murmurs
where
AS
AR
Transmitted to carotid, R2IS, best held on breath hold
AS
Crescendo-decrescendo systolic. In stenosis A2 is soft. AoScl not transmitted carotids. lub whoosh dub
AR
Early diastolic best heard leaning forward on breath hold (pulmonary diappears) lub tarrrr
aortic stenosis valve anatomy epi assoc pres O/E Ix mgmt comps
PRESSURE OVERLOAD
valve anatomy
three thin cusps
epi
most freq due to senile calc
assoc CAD bicuspid valve RF williams syndrome
pres
Classic triad: chest pain (predisposes to chest pain), heart failure (obstruction -> LV hypertrophy -> LV failure), syncope (insufficient blood)
SOBOE
O/E
Slow rising pulse
Narrow pulse pressure (diff between syst and dia)
LV hypertrophy -> apex thrill
Ejection systolic murmur that radiates to carotids
Crescendo-decrescendo early systolic murmur heard at R2IS transmitted to carotids
ix
ECG: LVH (*S wave V1 depth + R wave height V5/V6 > 35mm) or strain (ST depression and T wave inversion in lateral leads)
CXR: calcification of aortic ring, cardiac enlargement, post stenotic dilatation
*Echo (transthoracic): confirms presence + degree, + left ventricular function + thickness
Doppler echo for severity - pressure gradient > 50, area <1cm2 - reassess 6 monthly
mgmt
Avoid heavy exertion, modify RF for CAD
If symptomatic - prompt valve replacement - first line
If not fit for surgery
Second line - balloon valvuloplasty - risk of re-stenosis
TAVI - transcatheter aortic valve replacement
comp Predisposition to infective endocarditis Antibiotic prophylaxis Small emboli Decompensation - increased pressure in pulmonary - CHF Anticoagulate mechanical heart valves Target INR 2.5-3.5 for aortic Target 2-3 for others if no other risk factors (AF, previous stroke then 2.5-3.5)
aortic regurgitation causes age assoc pres O/E ix mgmt screening
VOLUME OVERLOAD
causes
Bicuspid aortic valve (congenital), rheumatic fever (@developing), infective endocarditis, collagen vascular disease, degenerative (@developed)
connective tissue disease RA/SLE
age
40-60 - degen
assoc
SLE, Marfan’s, Ehler-danlos, Turner’s, aortic dilatation with anky spon, acute AR in IE or aortic dissection (severe chest/back pain)
syphilis
HTN
pres
Acute - cardiovascular collapse
SOBOE/non specific or symptoms of left heart failure (orth, paroxysmal nocturnal dyspnoea)
O/E
Early diastolic murmur as R2IS sitting forward in expiration not well transmitted to carotids
Collapsing water hammer pulse
Wide pulse pressure
Austin Flint soft rumbling low pitched late diastolic murmur heard at apex
Quinckes sign - nailbed pulsation
de musset sign - head bobbing
ix
ECG - LVH (RV1 + SV5/6 >35mm)
CXR - ?signs of heart failure due to volume overload
TTE + colour doppler
mgmt
medical - LVH = diuretic, ACE i
Valve replacement
screening
Screen family members of patiens with Marfan’s
Mild - mod - review yearly + 2 yearly echo, severe i.e. left ventricular diameter/ejection fraction monitor 6 monthly
mitral stenosis patho causes pres O/E ix mgmt comp prevention
patho
Structural abnormality of valve -> increased LA pressure + pulmonary artery pressure
Pulmonary HTN -> RV dilatation and tricuspid regurg + RV failure
RV failure: raised JVP, liver congestion, ascites, peripheral oedema
static blood in LA = thromboembolism
causes
Congenital, rheumatic fever (most common), degenerative calcification (elderly) (SLE, RA, IE, amyloid)
pres
Asymptomatic for years then deteriorate
Progressive breathlessness (SOBOE, orth, PND), palpitations due to AF, systemic emboli
Symptoms due to enlarged LA - hoarseness, dysphagia
O/E
Malar flush (CO2 retention), raised JVP, RVH - laterally displaced apex/RV heave (4th intercostal tricusp), signs of RHF (hepatomegaly, ascites, peripheral oedema)
Mid-late diastolic murmur best heard in left lateral
Loud S1 with opening snap
low volume pulse
AF
ix
ECG: AF, large LA P-mitrale (bifid), RVH (dominant R wave in V1 >7mm tall, dominant S wave in V5/V6 >7mm deep)
CXR: LA enlargement, interstitial oedema (Kerley A/B lines), prominent pulmonary vessels
Echo -the normal cross sectional area of the mitral valve is 4-6 sq cm. A ‘tight’ mitral stenosis implies a cross sectional area of < 1 sq cm
mgmt
If AF: anticoagulant therapy indicated
For dyspnoea: diuretics (reduce preload) or nitrates
For exercise tolerance: BB or NDHPCCB
If symptomatic: Valve balloon: PMC percutaneous mitral commisurotomy
follow up yearly
comp
AF, pulmonary HTN, thromboembolism, RHF, rheumatic fever, IE
prevention
Prophylaxis for rheumatic fever and infective endocarditis (penicillin>)
mitral regurg def how it causes HF? epi causes RF pres O/E ix mgmt comps
def Mitral valve does not close properly causing leaking of blood from left ventricle back to LA
how it causes HF?
As the degree of regurgitation becomes more severe, the body’s oxygen demands may exceed what the heart can supply and as a result, the myocardium can thicken over time. While this may be benign initially, patients may find themselves increasingly fatigued as a thicker myometrium becomes less efficient, and eventually go into irreversible heart failure.
epi
Second most common, assoc females, low BMI, advanced age
cause
Now less rheumatic fever so most common cause is degenerative
MI, CAD, IE, post mitral valve surgery, Ehler-Danlos, SLE, rheumatic fever
RF Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome
pres
most asymp
Acute leads to rapid pulmonary oedema (papillary muscle rupture/IE) -> surgery
Chronic MR eventually causes heart failure and breathlessness, fatigue, oedema
O/E
Pansystolic blowing murmur at apex radiating to axilla
Laterally displaced apex beat
S3 gallop
ix
ECG: enlarged LA: broad P wave, AF
CXR: enlarged left atrium and left ventricle (cardiomeg)
Echo: confirm Dx and severity (based on jet into atrium)
mgmt
If signs of LV dysfunction or AF - surgery
med acute - Nitrates, diuretics, positive inotropes + intra-aortic balloon pump to increase CO
HF? ACEI, + BB + spiro
monitor 6 monthly
surg - If acute and severe
*Valve repair
comp pulm HTN LV dysfunction AF thromboembolism due to AF
rheumatic fever pathogenesis when occur what affected which valve RF pres criteria ix mgmt comp secondary prev
reaction to an infection
patho
Group A beta haemolytic streptococci (pyogenes)
Antigen mimicry - antibody to cell wall of strep cross reacts with valvular glycoproteins and cardiac myocytes -> inflammation and scarring
type 2 hypersensitivity
when?
2-4 weeks post streptococcal pharyngitis or skin infection
what affected? joints skin heart nervous system
which valve
90-95% mitral
RF
overcrowding
poor hygiene
skin infection
pres + criteria
3w post sore throat
JONES CRITERIA
Evidence of recent strep infection (e.g. scarlett fever, positive throat swab, increased/rising antistreptolysin O titre or DNase B titre)
Plus 2 major or 1 major + 2 minor
JONES PEACE
major:
Joints - large joint arthritis - NSAID (red, hot, swollen)
O (heart 40%) - carditis - pancarditis pericardium, myocardium, endocardium (valv), tachycardia, murmur, pericardial rub
Nodules (10%) painless and subcutaneous on extensors
Erythema marginatum (5%) - pale red macules/papules 1-3cm
Sydenham’s chorea (20%) jerking of upper limbs - purposeless
minor: PR interval prolongation (not if carditis major) ESR very raised Arthralgia (not if arthritis) CRP very raised Elevated temp (>90% are over 39 degrees)
ix
Evidence of streptococcal: throat culture, antistreptococcal antibodies (ASO, *anti-DNase B) rise during first month. Check 2 weeks apart for a rise
ECG: PR, ST elevation (saddle shape) suggests pericarditis
CXR - ?heart failure
FBC (WCC), ESR, CRP
Doppler echo for carditis
mgmt
Enforce bed rest till inflam markers normal
Eradicate strep - single IV benzylpenicillin + oral penicillin
Treat HF: diuretics, ACEI and digoxin
Suppress inflammation: NSAIDs
For chorea: self-limiting, may suppress with haloperidol (beware EPSE)
comp
carditis
mitral stenosis
congestive HF
secondary prev
abx proph - 5 yrs or till 21, 10 if carditis
infective endocarditis suspect when why affects valves organism RF pathogenesis course which valve pres dx ix mgmt comps
suspect when
fever
new murmur = endocarditis until proven otherwise
why affects vavles
Valves have a poor blood supply therefore it is hard for WBC and drugs to reach them
organism
Staphylococci (aureus) invasive procedures/drug users,
streptococcus viridans (subacute) (dental procedures)
staph epidermidis - most common cause following valve replacement
non-infective - SLE
rf Valve: rheumatic disease, replacement Congenital structural heart Previous IE Hypertrophic cardiomyopathy IVDU - tricusp
pathogenesis
All have non-bacterial thrombotic endocarditis (sterile fibrin-platelet vegetation) for adhesion and invasion
Invading organism clump and form thrombus and produce agglutinating antibodies
Organism destroys valve leaflets
Immune system activates forming immune complexes - cutaneous, kidney or arthritis
course
Acute - thrombus by invading org or valve trauma (wires)
Subacute - sufficient bacteria for invasion of thrombus
Non-bacterial - SLE, CKD, neoplasia
which valve
mitral > atrial > both
pres
Subacute: fatigue, low grade fever, polymyalgia, loss of appetite, wt loss
Acute: rapidly progressing infection
*Majority are fever + chills + poor appetite + wt loss
FROM JANE
Fever > 38 + tachycardia
Roth’s spots - eyes, retinal haemorrhage with pale centre
Osler’s nodes - painful red blisters @ terminal phalanges and toes
Murmur - Tricuspid with s.aureus
Janeway lesions - painless red maculae on thenar eminence
Anaemia/Arthritis: subacute = asymmetic > 3 jts, acute = septic monoarticular
Nail haemorrhage - splinter - red and linear
Embolic phenomena e.g. stroke
Subacute: clubbing
diagnosis
MODIFIED DUKES CLASSIFICATION
pathological criteria +ve
2 maj
1 maj + 3 minor
5 minor
PATHO
+ve histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
MAJOR:
1. Blood culture: 2 separate +ve blood cultures
2. Echo: evidence of endocardial involvement: vegetation/abscess
MINOR
1. Blood culture 1 +ve blood culture
2. Fever >38
3. Vascular phenomena: major arterial emboli, janeway lesions, IC haem
4. Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots, RF
5. Predisposition - IVDU, heart condition
ix FBC - wcc, anaemia ESR/CRP RF transthoracic echo within 24 hours blood cultures (subacute or chronic = 3 sets from peripheral sites within 6 hours between them, acute = start abx then take 2 within 1 hour) CXR ECG
mgmt
Start ABX empirical (IV)
General: amoxicillin + gentamicin for native valve
Severe sepsis: vancomycin + gentamicin
Prosthetic valve - vanco + rifampicin + low-dose gent
Confirm staph: 4W IV flucloxacillin (or vancomycin +rifampicin if MRSA)
Confirm strep 4W IV benzylpenicillin + low dose gent
indications for surg:
- severe valvular incompetence
- aortic abscess (often indicated by a lengthening PR interval)
- infections resistant to antibiotics/fungal infections
- cardiac failure refractory to standard medical treatment
- recurrent emboli after antibiotic therapy
comps MI percarditis glomerulonephritis stroke + otehr embolic phenomena s.aureus most common - tricuspid murmur
proph
abx for those at high risk undergoing dental procedures
cardiomyopathy def classification epi gen ix gen mgmt
def Myocardial disorder in which heart muscle is structurally and functionally abnormal without CAD, valvular disease, HTN, congenital
classification 1
PRIMARY
SECONDARY from:
Impaired LV function: CKD, cirrhosis, stress
Multisystem disease: sarcoid, amyloid, SLE
Endocrine: diabetes, thyroid
Drugs: alcohol, cocaine abuse
classification 2
1. Dilated - *most common, left or both ventricles dilated with impaired contraction
Ischaemic, alcoholic, thiamine def (Beri-beri), coxsackie, chagas, SLE
2. Hypertrophic - 2nd common, left/right ventricular hypertrophy, usually familial (AD) - beta myosin
3. Restrictive - rare, reduced diastolic filling with near normal systolic function e.g. amyloid, fibrosis, sarcoidosis, radiation, haemochromatosis, Loefflers
epi
Can occur at younger age *suspect this at a young person presenting with heart failure, arrhythmia or thromboembolism
gen ix
Bloods: FBC, ESR, U+E, LFT, cardiac enzyme, TFT
CXR
ECG: usually abnormal
Transthoracic doppler echocardiography: can confirm Dx of hypertrophy and exclude valvular
MRI: to distinguish constrictive and restrictive disease
gen mgmt
Often symptomatic: treat heart failure and prevent thromboembolism and sudden death
If high risk arrhythmia consider implantable cardioverter defibrillator
All require thorough assessment of functional capacity and cardiac function
management of irregular narrow QRS tachycardia
more than likely AF
- ABCDE
- 02 + IV access
- monitoring on - ECG, BP ,02 + record 12 lead ECG
- identify + treat reversible causes eg electrolytes
ANY ADVERSE FEATURES? yes -> 3 SHOCKS -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours
NO ADVERSE FEATURES -> control rate with BB or diltiazem, consider dig or amiodarone if evidence of HF
management irregular broad complex QRS tachycardia
GET EXPERT HELP ASAP
- ABCDE
- 02 + IV access
- monitoring on - ECG, BP ,02 + record 12 lead ECG
- identify + treat reversible causes eg electrolytes
ANY ADVERSE FEATURES? yes -> 3 SHOCKS -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours
NO ADVERSE FEATURES -> potential causes: AF with BBB - > as for narrow complex pre-excited AF -> consider amiodarone polymorphic VT (TDP) -> magnesium 2g over 10 mins
management of regular broad complex QRS tachy
- ABCDE
- 02 + IV access
- monitoring on - ECG, BP ,02 + record 12 lead ECG
- identify + treat reversible causes eg electrolytes
ANY ADVERSE FEATURES? yes -> 3 SHOCKS -> amiodarone 300mg IV over 10-20 mins + repeat shock -> amiodarone 900mg over 24 hours
NO ADVERSE FEATURES ->
VT or uncertain -> amiodarone 300mg IV over 20-60 mins then 900mg over 24 hours
prev confirmed SVT with BBB -> give adenosine as for reg narrow tachy
dilated cardiomyopathy what is it causes pres ix mgmt comp
what is it all 4 chambers dilated Ventricular chamber enlargement + contractile dysfunction with normal LV wall thickness due to biochemical abnormality of cardiac muscle. causes systolic dysfunction MOST COMMON - 90%
causes idiopathic Ischaemia, HTN doxorubicin - drug genetic (AD) - duchenne musclar dystrophy *alcoholism, thyrotoxicosis, SLE/RA, coxsackie, thiamine -Beri beri *cocaine abuse
pres Symptomless to sudden death *Heart failure - congestive: L (dyspnoea, fatigue, orthopnoea, PND) R (oedema, JVP, ascites) + 3rd/4th heart sound + cardiomegaly (displaced apex) Arrhythmia - AF or *VT Thromboembolism - by stasis
ix
CXR: CHF: ABCDE (alveolar oedema - bat wing, kerley B - interstitial, cardiomegaly (balloon like heart), dilated upper lobe vessels, pleural effusion)
ECG: sinus tachycardia, LBBB or non-specific T or ST change, or *AF
Echo: marked dilatation LV, reduced systolic/diastolic function, MR or TR, mural thrombus
Bloods: BNP: for heart failure
Potential biopsy for amyloid, sarcoid
mgmt aim = improve cardiac function furosemide ACEi/ARB + BB - reduce LV EF treat AF further - biventricular pacing of class 3/4 HF, ICD if high risk VT
comp
progressive HF
sudden death from ventricular arrhythmia
Hypertrophic cardiomyopathy what is it causes assoc leads to epi pres O/E ix mgmt
what is it
LVH, mitral valve abnormalities, impaired diastolic filling, disorganised cardiac myocytes (disarray) and fibrosis on biopsy
predom diastolic dysfunction
causes
AD genetic inheritance, mutation in gene coding for beta-myosin or troponin
assoc
Mitral regurgitation, AF in 20%
friedreichs ataxia
WPW
leads to
Dynamic obstruction of LV outflow tract, myocardial ischaemia, SV/V tachyarrhythmia
epi
*Most common cause of sudden cardiac death in young people and athletes due to arrhythmia or obstruction of LV outflow tract
pres 20-30s mainly asympt Dyspnoea, chest pain, palpitations, syncope typically following exercise due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis (from arrhythmia and outflow tract obstruction) sudden death - vent arrhythmias
O/E
Forceful apex beat, *double impulse if LVOTO
Harsh ejection systolic murmur *augmented by standing or Valsalva LVOTO @left sternal edge radiating to mitral and aortic area ± mitral regurgitation murmur
jerky pulse
ix
ECG:
LVH: *S wave V1 depth + R wave height V5/V6 > 35mm
Ischaemic changes: ST segment changes, T wave inversion
deep Q
Left axis deviation
AF (20%)
Most common arrhythmias are premature ventricular complexes (above)
Echo: *Diagnostic: Transthoracic echo: LV thickening (<20mm = low risk) mnemonic - MR SAM ASH mitral regurgitation (MR) systolic anterior motion (SAM) of the anterior mitral valve leaflet asymmetric hypertrophy (ASH)
CXR - atrial enlargement if mitral regurgitation, variable cardiomegaly
Genetic testing
Endocardial biopsy for amyloid causing thickening
mgmt - ABCDE + others
Amiodarone or catheter ablation
BB or CCB - verapamil or diltiazem for reduce ventricular contractility which decreases LVOT gradient
Cardioverter defib - if risk of sudden death
Dual chamber pacemaker
Endocarditis proph
rx AF if LVOT high - septal myectomy genetic counselling avoid competitive sport avoid nitrates, ACE-i, inotropes
restrictive cardiomyopathy what is it epi assoc ddx causes pres ix mgmt
what is it
Normal LV cavity size and systolic function but increased myocardial stiffness therefore mainly fills in early diastole (reduced) leading to increased atrial pressure
epi
old
assoc
AF
ddx
constrictive pericarditis
causes Endomyocardial fibrosis (Lofflers), *amyloid (worst), sarcoid, haemochromatosis, rad
pres
- Usually present with HF but normal systolic i.e. dyspnoea, fatigue, loud S3, pulmonary oedema, murmur
- Features of RVF predominate: raised JVP, hepatomegaly, oedema, ascites
- *v. similar to constrictive pericarditis: Kussmaul’s sign (increased JVP with inspiration), pulsus paradoxus (decreased pulse + BP at inspire)
ix CXR: ABCDE ECG: low voltage complexes Echo: non-dilated, non-hypertrophied ventricles, atrial enlargement, sparkling@amyl *Cardiac catheterisation for pressures
mgmt
Manage heart failure, amiodarone for ventricular arrhythmia, anticoagulate (AF), BB and CCB for rate control AF, transplantation sometimes indicate
myocarditis what is it pres causes ix mgmt comp
what is it
acute or chronic inflam of myocardium
pres MI + FEVER usually young patient fatigue chest pain arrhythmias
causes
*Viral infection fever, malaise, lethargy, fatigue
Coxsackie B virus, HIV
diphtheria
Immune mediated: SLE, sarcoidosis, scleroderma
Toxic: alcohol, heavy metals
Electric shock
ix
FBC - leukocytosis, ESR or CRP (75%), Cardiac enzymes: CK, TrI, TrT, BNP raised
+ve Viral serology
*Gold standard - endomyocardial biopsy
Cardiac MRI may differentiate transient and permanent tissue damage therefore good to diff from infarction
ECG: ST elev/dep + T wave inversion, tachycardia
CXR: normal cardiac silhouette but other signs of heart failure
mgmt
Treat cause: viral = supportive + bed rest
If acute: i.e. fever, flu-like, WCC + haemodynamic compromise to ITU
Symptomatic hypotension: +ve inotropes i.e. phosphodiesterase inhibitors or dopamine
Anticoag if AF
comp
CHF, pulmonary oedema, cardiogenic shock
what drugs should you avoid in heart failure
flecainide CCB lithium NSAIDs drugs prolonging QT - erythromycin
Acute LVF what is it causes pres O/E ix mgmt
what is it
life-threatening emergency
AHF without a past history of heart failure is called de-novo AHF. Decompensated AHF is more common (66-75%) and presents with a background history of HF.
AHF is usually caused by a reduced cardiac output that results from a functional or structural abnormality.
causes - CHAMP coronary syndrome hypertensive emergency arrhythmia mechanical - acute valve leak, VSD, LV aneurysm P.E
PRES
patient looks acutely unwell - pale and grey
cold clammy peripheries
?cyanotic
frothy blood stained sputum in a pot - ‘pink’
orthopnoeic using accessory muscles
cardiac asthma - wheeze
O/E
sinus tachy or AF
systolic hypotensive
signs of cardiomegaly - displaced apex, signs of valve disease
third and fourth heart sounds
right sided or bilateral pleural effusions
ix
FBC - anaemia as cause
U+E, creatinine - for diuretics
blood glucose
B-type natriuretic peptide - raised level confirms diagnosis
ABG - hypoxic? resp acidosis?
trop - rule out infarction
ECG - arrhythmia, heart block, ischaemia, ventricular hypertrophy
ECHO - within 48 hour for evidence of reduced ejection fraction and valvular heart disease
CXR - Aveolar effusion, B- kerley B lines (fluid in septal lines)/bats wings (prominent hilar shadows), cardiomegaly, diversion of upper lobes/diffuse mottling of lung fields, Effusion in interlobar fissures
mgmt Pour SOD Pour away their IV fluids aka STOP Sit up Oxygen Diuretics - IV furosemide 40mg stat
other thing to consider - IV pain killer (opiates are vasodilators so be careful), NIV or CPAP, inotropes (dobutamine) if systolic <90.
might need vasodilators if systolic <90 = GTN or isosorbide mononitrate
Acute LVF patho
This occurs when the left ventricle is unable to adequately move blood through the left side of the heart and out into the body. This causes a backlog of blood (like too many buses waiting to pick up people at a bus stop) that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues. This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid. This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms.
what can also cause a raised BNP
sepsis tachycardia pulmonary embolism renal impairment COPD
chronic heart failure what is it causes pres - R + L O/E ix mgmt prognosis
what is it
It is caused by either impaired left ventricular contraction (“systolic heart failure”) or left ventricular relaxation (“diastolic heart failure”). This impaired left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart
causes
Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
pres
RHF: peripheral oedema, abdo distension (ascites), facial engorgement, pulsing in neck and face (tricuspid regurg)
LHF: dyspnoea, fatigue, cold peripheries, muscle wasting, orthopnoea, PND, nocturnal cough - pink frothy sputum
O/E - Tachypnoea, tachycardia, cool peripheries, cyanosis, displaced apex (LV dilatation), RV heave (pulmonary HTN), raised JVP
Cardiac asthma: bilateral basal end-inspiratory crackles ± wheeze
Peripheral oedema, tender hepatomegaly (pulsatile at TR)
Gallop rhythm due to S3 or murmur of mitral or aortic valve diseas
ix
first line blood test - N-terminal pro-B-type natriuretic peptide:
- if levels are ‘high’ >2000pg/ml arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
- if levels are ‘raised’ 400-2000pg/ml arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
ECHO - function - reduced ejection fraction or valvular disease
12 lead ECG -
CXR
FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, consider cardiac enzymes
mgmt
ACE-i lisinopril 2.5mg daily + BB bis 1.25mg daily
intolerant of ACE -> ARB - candesartan 4mg daily
intolerant of ARB -> hydralazine or nitrate
increases doses for clinical effect
if @ max and no effect + aldosterone receptor antagonist eg spiro 25mg daily
refer for consideration of sacubitril valsartan, dig, ivabridine, resynch therapy
Lifestyle (ex, smoking, alc, diet), patient education, depression
Annual influenza vaccination, pneumococcal vaccination (once only) - prophylactic
Inform DVLA, air travel likely ok
Manage comorbities: HTN, prevention MI, diabetes
prognosis
50% die within 4 years, worse prognosis if reduced ejection fraction
classification of heart failure
NEW YORK HEART ASSOCIATION STAGING SYSTEM
Class I asymptomatic on normal physical
Class II slight limitation no restriction flying
Class III less than ordinary activity - symptoms oxygen may be required
Class IV inability to carry out any activity - symptoms oxygen recommended
explain normal ejection fraction
this is the percent of blood that is pumped out of the left ventricle after each contraction
An ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out with each heartbeat
normal = 50-70
too high = >75 - hypertrophic cardiomyopathy
too low <40 = HF or cardiomyopathy
40-50 = borderline
define atherosclerosis
and the steps of atherogenesis
def Complex inflammatory process characterised by accumulation of lipid, macrophages + smooth muscle cells within intimal plaques
steps
1. Fatty streak formation: Endothelial dysfunction -> increased permeability to fat and monocyte infiltration -> taken up by MP to make foam cells -> fatty streak
Fatty streak progresses -> transitional plaque
2. Intimal hyperplasia: PDGF, TGF-B by macrophages, monocytes and damaged endothelium -> further accumulation of macrophage and smooth muscle cell proliferation
3. Fibrous cap: smooth muscle produces collagen
4. Plaque formation, or rupture may have fatty necrotic core
The plaque may narrow the lumen or become unstable and rupture
cholesterol
name of pathway
HDL +LDL
where is it taken and used
mevalonate pathway
HDL + LDL
HDL - good cholesterol carries LDL away from arteries, LDL - bad cholesterol blocks arteries
where
Cholesterol -> liver (synthesis of bile salts) or endocrine glands (synthesis of steroids)
statins mechanism when do NICE recommend them SE dose monitoring
mechanism
HMG-CoA reductase inhibitors
when do NICE recommend QRISK2 > 10% (10 year risk) - primary prevention if <84 History of CVD Familial hypercholesterolaemia Anyone over 85
SE
Myalgia, stiffness, weakness, cramping (usually at around 6 months)
dose
Atorvastatin 20mg for primary prevention, 80mg for secondary
monitoring
LFT
HTN RF stages screening what does 10mmhg reduction = causes how to calc HTN CRISIS ?phaeo end organ damage pres ix management pathway
RF
Modifiable: smoking, weight, alcohol, stress, exercise, dietary salt
Non-modifiable: old, fam Hx, ethnicity, gender
stages
Stage 1: >140/90 or >135/85 on ABPM or HBPM (ambulatory)
Stage 2: >160/100 or >150/95
Stage 3: >180/110
screening
Often symptomless screen every 5 years for adults up to 80 then annually
-10mmhg = Decreases risk heart disease risk of cardiovascular event 20%
causes
PRIMARY - essential
SECONDARY -
Renal disease: intrinsic (75%) i.e. glomerulonephritis, polyarteritis nodosa, systemic sclerosis, PCKD, or renovascular renal artery stenosis -> increased renin by decreased perfusion
Endocrine: cushings, conns, thyroid, phaeo, acromegaly, hyperparathyroid, primary hyperaldosteronism
Coarctation aorta
Pre-eclampsia and pregnancy
Drugs - decongestants, COCP, steroids
calc
BP = CO X TPR
HTN crisis
Malignant/accelerated hypertension (syst>200 or dia>130) + evidence of end-organ damage: *same-day assessment and immediate treatment (dec BP in hours)
Hypertensive urgency (syst>180, dia>120) without end-organ damage, may dec BP over days
suspect phaeo
Labile or postural hypotension + headache, palpitations, pallor, sweating
end organ damage Brain - Encephalopathy: seizure, vomiting, nausea Dissection - delayed/weak femoral pulses Pulmonary oedema - heart failure Nephropathy - proteinuria ± loin bruit Eclampsia Papilledema Retinopathy (hypertensive) - Grade 1: tortuous retinal arteries + silver wiring - Grade 2: AV nipping - Grade 3: flame haemorrhages and cotton wool spots - Grade 4: papilloedema
pres often asymp unless >200/120 headache visual disturbance seizure cushinoid conns - tetany, weak muscles, polyuria, hypokalaemia, thyroid, phaeo
ix
24 hour BP
following diag:
urea and electrolytes, creatinine: check for renal disease, either as a cause or consequence of hypertension
HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease
lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease
12 lead ECG
urine dipstick
?renal USS
fundoscopy
mgmt lifestyle >135/85 rx with antihypertensive if >150/95 or >135/85 with: - age >80 with clinic >150/90 - age <80 with target organ damage, CV or renal disease, diabetes or 10yr CVD risk >10% MEDICAL MGMT T2DM <55 OR WHITE = 1. ACEi or ARB 2. +CBB or thiazide like diuretic 3. ACE-/ARB + CCB + thiazide like
55+ OR BLACK =
- CCB
- +ACEi or ARB or thiazide like
- all three
PREGNANT = labetalol 100mg BD for mod HTN
FINAL STEP FOR BOTH = confirm resitance + check for postural + discuss adherence
seek expert advice
add low dose spiro if k <4.5
alpha blocker or BB if k >4.5
monitoring
use clinic BP
measure sitting/standing in people with T2DM or postural hypo or >80
IHD rf
Multifactorial: genetic, lifestyle, environmental
Modifiable: low SE status, smoking (60% higher), poor diet (high trans-fatty acid, low fibre, low fruit and veg), weight, low exercise, alcohol, stress and depression, *HTN (every 20/10 doubles risk of death), *cholesterol/hyperlipidaemia, *diabetes
Unmodifiable: age, male, south asian, family Hx MI = x2, previous Hx, +ve family history <55 men or < 60 women, metabolic syndrome
stable angina def cause variants rf pres ddx ix mgmt
def Chest pain or discomfort resulting from decreased blood supply to heart muscle, myocardium (ischaemia) without infarction
cause
Usually due to narrowing of lumen of CAD due to atherosclerosis or thrombosis
variants
Decubitus (on lying down)
Prinzmetal’s (at rest as a result of CA spasm)
Stable - pain precipitated by predictable factor: exercise/emotion
Unstable - angina occurs at any time, manage as ACS
rf
As before + cardiac abnormalities e.g. outflow obstruction (Aortic Stenosis) or hypertrophic obstructive cardiomyopathy
pres
1 - constricting discomfort in front of check, neck, shoulders, jaw, arms
2 - precipitated by physical exertion
3 - relieved by rest or GTN in *5 minutes
*typical if all, atypical if 2/3, non-anginal = 1 or 0
ddx
Pain over 5 mins - MI
Acute pericarditis - worse on inspiration, lying flat, swallowing
MSK - worse on mvmt
GORD
Pleuritic pain - sharp pain on deep inspiration, ?pneumonia or PE
ix 12 lead ECG - ischaemic changes @ exercise stress test - ST/T wave flattening or inversion FBC glucose chol/triglycerides LFTs - baseline before starting statin U/E TFT estimate likelihood of CAD - all men >70 = 90%, w >70 = 60-90 unless high risk >90 = manage as angina 60-90 = invasive coronary angiography 30-60 = non-invasive functional imaging - stress echo 10-30 - CT calcium scoring <10 - reconsider Dx
mgmt
REFER ALL ?ANGINA to rapid access chest pain clinic for confirmation of dx and severity assessment - within 2 weeks
modify RF - patient edu
advice on stopping activity and GTN spray, if pain doesn’t ease 2nd dose @ 5 minutes, 3rd dose @ 5 minutes, wait 5 minutes then 999 (i.e. after 15 mins total)
PHARMA -
Short acting nitrate: GTN
First line anti-anginal: BB (atenolol, lower HR and BP, bradycardia, cold hands/feet, fatigue) or CCB (diltiazem/verpamil/amlodipine - ankle swelling, flushing)
Second line: combination - *must be dihydropyridine CCB + BB
If intolerant or CI: consider long acting nitrate or nicorandil or ivabradine
Vasodilation - CCB and nitrates, cardiac depressants - BB and CCB
Aspirin 75mg or clopidogrel- antiplatelet (establish bleeding tisk), statin if indicated, ACE-I for HTN/diabetes
Review at 2-4 weeks
if not controlled on medicine = CABG or PCI
classifying ACS
trop neg = unstable angina
trop posi = NSTEMI/STEMI
ACS diagnosis chest pain suspect ACS if rf initial ix mgmt of STEMI mgmt NSTEMI comps of MI
diagnosis two of three: 1. cardiac chest pain 2. positive trop 3. ECG changes - T wave inversion, ST elevation/dep, Q waves, new LBBB
chest pain central restrosternal band-like constriction non-pleuritic radiates to left
suspect ACS if: lasts longer than 15 mins occurs @ rest - unstable angina increasing in freq - cresendo angina severe - associated with n + v or sweating, non-resolving with nitrates
rf smoking HTN DM hyperlipidaemia FH CKD
ix
FBC - anaemia
U and creat - impaired renal function can cause false posi elevation of trop, baseline levels required prior to ACE inhib
electrolytes - hypokalaemia, hyperkalamia
glucose
LFT- baseline for statin, impaired = CI for ticagrelor
lipids
serial trops
ECG - Q waves imply full thickness infarct, without = subendocardial
mgmt STEMI
with para - morphine + cyclizine, oxygen, nitrates
ABCDE + o2
aspirin 300mg oral
PPCI <12 hours since symps, <2hrs since arrival (if not poss then consider fibrinolytics eg altepase) - will be given loading dose of prasugrel prior
follow up = ABCDE
ACE-i
BB
Cholesterol lowering, high dose statin is also plaque stabilising
Dual antiplatelet therpy - aspirin 75mg indef + prasugrel for at least one year
Echo - to assess LV
mgmt NSTEMI/unstable angina
para give o2, GTN, morphine
ABCDE
aspirin 300mg stat
risk stratify based on 6/12 mortality
lowest risk <1.5 = aspirin, review as outpatient, ?exercise ECG, ?Angiogram
low risk - 1.5-3% = fondaparinux, conservative - review as outpatinet ?exercise ECG, ?, Angiogram , aspirin + ticagrelor or clopidegrel
intermediate >3% and high >6% = unfractionated heparin, early invasive mgmt PPCI -> aspirin + prasugrel if stented
comps
pump failure
ruptureof papilary muscle or septum
aneurysm and arrhythmias
embolism -> mural thrombus -> stuck on wall
dresslers syndrome (late 4-6 w later sharp pain = POST MI SYNDROME) - plus early acute pericarditis (doesnt respond to opioids
SIX QUALITIES of pericardial pain
sharp, worse on insp retrosternal, radiates to left (shoulder) worse on lying flat eased by sitting up
what does the ST elevation indicate
and findings that confirm it
current injury
usually implying occlusion by ruptured plaque with in-situ thrombosis
> 1mm in limb or >2mm in 2 adjacent chest leads OR new LBBB
how to assess risk of future CVE (6 month mortality)
GRACE - global reg of acute cardiac events)
Risk and Mortality Calculator
looks at age HR BP trop HF creat
driving after MI
*Post ACS = 4 weeks off driving, 1 week if treated by angioplasty
cardiac arrest management
999
A+B (if breathing turn to recovery)
C - CPR 30:2, when airway secured = uninterrupted compressions and ventilate at 10/min
D defibrillator: AED automated external defibrillator
Complete 2 minutes of CPR between debif attempts
After 3rd shock give adrenaline + amiodarone
2 minutes CPR
Adrenaline
2 minutes CPR
Adrenaline
acute pericarditis what is it pathogenesis causes when granulomas - cause pres O/E ix mgmt comps
what is it
Outer fibrous layer (parietal pericardium) and inner serous membrane (visceral pericardium) with 50ml fluid between
Limits dilation, maintains ventricular compliance (Starling), fixes heart to sternum
pathogen
Inflammation of pericardium - pericardial vascularisation and infiltration with polymorphonuclear lymphocytes. Fibrinous reaction results in exudate and adhesions within pericardial sac and serous/haemorrhagic effusion develops
causes Viral: *coxsackie, EBV + staphylococcal/haemophilus... Rheum: *SLE, sarcoid + …. Post MI: *Dressler’s 24-72 hours Drugs: hydralazine Other: *uraemia
when granulomas
TB, sarcoid, fungal, RA
pres
*Chest pain
Dull, sharp, burning, pressing (up to severe)
Felt substernal or precordial
Radiates to neck or left trapezius
*Aggravated by inspiration, cough, swallow, lying flat
*Relieved by sitting up and lying forward
O/E
60-85% pericardial friction rub - scratchy, louder in inspiration, heard at midline
Tachypnoea, tachycardia, fever
If *tamponade -> may exhibit Beck’s triad:
Hypotension, elevated systemic venous pressure (JVP), muffled heart sounds
If slow develop pulsus paradoxus - 10mmHg fall in SBP with insp
ix
Serial ECGs:
Stage 1, diffuse concave ST segment elevation (saddle shape) with concordance of T waves, PR depression. Stage 2, return to normal and T wave flatten. Stage 3, T inversion. Stage 4, resolution of T wave.
CXR: globular heart if > 250ml
FBC (WCC), ESR/CRP (raised) U+E (uraemia?) cardiac enzymes (if MI)
Echo - *if suspect effusion or tamponade (>20mm free fluid)
*if suspect impending tamponade (RA or vent diastolic collapse on echo) - pericardiocentesis
mgmt
Stable: rest + treat cause + NSAIDs (naproxen) ± PPI, (if uraemic consider dialysis) + colchine
Admit if fever, evidence tamponade, a large effusion (echo free space > 20mm), on warfarin, trauma, fail to respond NSAIDs
comps
*falling blood pressure and shock - suspect cardiac tamponade - immediate peircardiocentesis with echo
Chronic + symptomatic - pericardial resection
Recurrent: colchicine in addition to NSAIDs
becks triad
cardiac tamponade
hypotension
raised JVP
muffled heart sounds
cardiac tamponade what is it pres patho ix mgmt
what is it
Collection of blood/fluid/pus/gas in the pericardial space. A large volume will result in reduced ventricular filling leading to haemodynamic compromise
MEDICAL EMERGENCY
pres
Anxiety, fatigue, oedema, dyspnoea, tachyc, tachyp
O/E: Beck’s triad if acute (muffled, JVP, hypotension) + distended neck veins, hepatomegaly, tachyc/p, pulsus paradoxus (*exaggeration of normal decrease in BP on inspiration, distinguish CT from pericardial effusion)
patho
On inspiration decrease ITP -> increased flow to RH -> pressure transmitted to septum which impairs LV filling
ix
ECG - Low voltage QRS complex. Electrical alternans. Amplitude increases and decreases beat to beat QRS
CXR - Cardiomegaly, water-bottle shaped heart, calcification @ restrictive
transthoracic echo - gold standard
mgmt
O2 + volume expansion + increase venous return (legs up) + inotrope (dobutamine) + pericardiocentesis
aortic dissection def course loc rf pres ix worry about mgmt
def Intimal tearing lead to disruption of media provoked by intramural bleeding. This leads to separation of the layers and formation of a false lumen
course
Acute < 14 days, subacute 15-90, chronic >90
location Type A (70%) - aortic arch and ascending aorta proximal to *L subclavian Type B (30%) - descending aorta distal to L subclavian
RF
CV RF + aortic disease + cocaine/amfetamines + M/ED + bicuspid valve
pres
Initial phase: Sudden tearing/sharp pain radiating to back, pulse loss
Expansion phase: pressure increase causes rupture to pericardium (tamponade), or pleural space or mediastinum
*Pain maximal at onset, migrates as dissection progresses
To spinal arteries - paraplegia
To distal aorta - limb ischaemia
To carotids - neurological deficit
To coronary - angina
ix BP in both arms differentiate from MI ECG CXR - widened mediastinum TTUS - site + extent MRI for diagnosis + identification of other vessels
worry about - rupture, multi-organ failure, cardiac tamponade, hypotension
mgmt IV access ABCDE analgesia ICU mgmt HTN aggressively - IV BB (labetalol) to reduce ventricular contraction, IV nitroprusside (emergency vasodilator) SURGERY - typeA to prevent rupture - graft type B - TEVAR
Thoracic aortic aneurysm def types area affected pathogenesis causes rf pres ix mgmt monitoring
def Permanent and irreversible dilatation of bv by > 50% of normal diameter. True aneurysm involves all three layers
types thoracic abdominal - the maj ruptured 26-28mm
areas affected Acending aorta (51%), aortic arch, descending aorta (n.b. Aortic hiatus of diaphragm is at T12)
pathogen
Complicated: inflammation, proteolysis and reduced survival of smooth muscle cells
causes
Genetic/familial (AD for TAA)
Connective tissue: Marfan’s, Ehler Danlos
Infection: HIV, syphilis
Aortitis: GCA, RA, takyasu’s arteritis
Trauma, weight lifting, cocaine, amfetamine (due to BP rise)
RF
Turner’s, COPD, CKD, HTN, age, smoking, atherosclerosis, bicuspid aortic valve
pres
Pain: chest, neck, upper back, mid back, epigastrium, acute - rupture imminent? dissection is sudden, tearing
Symptoms due to local compression: hoarseness, cough, stridor, dyspnoea, SVC obstruction, dysphagia
If rupture: acute pain + collapse/shock + aneurysm erosion into local structure: haematemesis (aorto-oesophageal fistula), haemoptysis (aorto-bronchial), haemothorax, cardiac tamponade
ix
Acute: FBC, clotting, renal/liver, cross-match, ECG, CT contrast, MR angiography
Chronic: FBC, ESR/CRP, LFT/amylase, ECG, LuFT, USS, *TTE, *AUS (for AAA) CT angiography, MR angiography (for cause, infective, inflammatory, pancreas (DDx))
mgmt
Surgery: *graft insertion or TEVAR (thoracic endovascular aneurysm repair)
if symptomatic *regardless of size or Marfans
Ascending > 5.5cm, descending >6cm
comp - paraplegia due to spinal ischaemia, stroke, AKI
Medical: smoking cessation, treat 2nd RF CVD
if marfans - Require lifelong BB, regular imaging of aorta and restriction physical activity
monitor
6 monthly MRI/CT and inform DVLA above certain size
rupture of AAA pres ix mgmt prog
pres
Thoracic: chest pain indistinguishabe from MI + haemoptysis ± cardiac tamponade
Abdominal: classic triad: flank/back pain, hypotension, pulsatile abdominal mass
Pale + sweaty, weak thready pulse, hypotension
ix
FBC (Hb will be normal, high WCC), group and save/crossmatch, baseline U+E
CXR, AXR (75% are calcified)
ECG for MI
mgmt
Large bore IV access
Group and crossmatch, order 4-6 units blood, FFP, Pt
Immediate theatre
Secure proximal aortic control
Prosthetic graft repair and stem bleeding - EVAR
prog
only 1 in 3 reach hosp alive
shock
types
why it kills
at risk organ systems
types
hypovolaemic - loss of blood/fluid
cardiogenic - hf, heart cant pump to maintain CO
distributive - anaphylaxis, sepsis, neurogenic
obstructive - PE
why it kills
Triad of coagulopathy, hypothermia, metabolic acidosis -> leads to compensatory tachypnoea
at risk organs
Kidney (acute tubular necrosis), lung (ARDS), heart (MI), brain (confusion, irritability coma)
hypovolaemic
ix
staging
mgmt
ix
Hb, UE, LFT, group and crossmatch, ABG + lactate, monitor urine
staging
Class 1: 10-15% physiological compensation
Class 2: 15-30% postural hypotension, urine to 20-30ml/Hr
Class 3: 30-40%tachycardia >120, urine under 20, confused
Class 4: 40% marked hypotension, tachycardia, tachypnoea, no urine, comatose
Compensated baroreceptors result in increased myocardial contractility, tachycardia and vasoconstriction. Maintain BP. Release vasopressin, aldosterone, renin
Progressive/uncompensated with myocardial depression, failure of vasomotor reflex, increased capillary permeability and lactic acidosis
Irreversible: failure of vital organs
mgmt
Raise legs
ABCDE
Crossmatch + blood for Ix as previous + catheter + ABG
Airway + high flow O2 + 2 large bore IV cannula
Fluid resus saline or Hartmann’s 500ml over 15 mins *may give 2l total then escalate
If haemorrhagic shock give blood as soon as possible O-ve
Pain relief - pain increases metabolic rate and increases ischaemia IV opiates
*vasopressors cause further tissue ischaemia
Surgery to stem blood loss: e.g. REBOA after res
cardiogenic shock
cause
mgmt
cause
Most often caused by acute MI (affecting anterior wall) - or pericardial tamponade/severe constrictive pericarditis or obstructive PE or tension pneumothorax
mgmt
A+B - intubation ± mechanical ventilation, O2
C - gain venous accessl often require central venous access as peripherally shut down - send bloods
IV fluid if depleted volume 250ml bolus (cardiac dysfunction)
Monitor - cardiac monitoring, BP - art line, venous pressure - CVC, urinary catheter
Ix: UE, preg, FBC, ABG, BNP, ECG, CTPA, CXR
Pain relief *IV morphine and cardiac inotropes *dopamine or dobutamine
Revascularisation
anaphylactic shock
def
pres
mgmt
def Systemic hypersensitivity: sudden onset, rapidly progressing, life threatening
pres Profound vasodilation (warm peripheries, low BP, tachycardia) Breathless/wheeze Urticaria/hives/angio-oedema *Oedema of face, pharynx, larynx
mgmt
A (call for help if any signs of obstruction) B (treat resp distress) C (colour, pulse, BP) D (responsive?) E
High flow O2
Lie flat and raise legs
IM adrenaline *0.5mg adult, child: >12 = adult, 6-12 = 300mcg, <6 = 150mcg
Expert intubation
IV fluid challenge: large bore cannula: 500ml crystalloid in 5-10 mins, 250ml if known heart failure
IV chlorphenamine + hydrocortisone
Bronchodilators: salbutamol IV or nebulised, ipratropium inhaled, aminophylline IV
septic shock sepsis 3 def pres mgmt comps
Life threatening organ dysfunction due to a dysregulated host response to infection
Clinical criteria: organ dysfunction defined as an increase of 2 points or more on SOFA score - mortality rate 10%:
qSOFA - HAT
- Hypotension - < 100mmHg
- Altered metal state - GCS < 15
- Tachypnoea - >=22
pres
Bounding pulse, temperature, rigors, rapid capillary refill, vasodilation, warm peripheries
mgmt Blood cultures + septic screen, U+E Urine output - monitor hourly Fluid resuscitation Antibiotics - tazocin? gent? according to local guidelines Lactate, ABG/VBG Oxygen to correct hypoxia refer to ITU for inotropes
FBC, UE, urine dip, LFT, glucose, *clotting inc D-dimer and fibrinogen for DIC, CXR, AUSS - find the infection
Complications DIC, renal failure, cardiorespiratory failure
critical limb ischaemia timeline, ABPI + mortality
chronic limb ischaemia - intermittent claudication (not progressive, ABPI >0.4, 1 year mortality 4%
critical limb ischaemia - rest pain requiring opiates for >2/52 or evidence of tissue necrosis, ulceration or gangrene, ABPI <0.4, 1 year mort 12%
acute limb ischaemia (thrombosis or embolus) - sudden decrease in limb perfusion that causes a threat to limb viability, 6Ps - pale, pulseless, painful, parasthesia, paralysed, perishingly cold, ABPI <0.1, 1 yr mort 20%
what do you have to remember with diabetics with peripheral vascular disease
they have abnormally high ABPI’s due to calcified vessels
arterial ulcer characteristics
ddx
CI
small and painfull over pressure-points: back of heel, plantar aspect of big toe
punched out margin
at ankle, typically over lateral malleolus
associated with cold foot, absent pulses and low ABPI
ddx
neuropathic ulcer - are painless and foot is warm with reduced sensation
venous ulcers typically on medial calf or ankle with associated skin changes
10% of ulcers are mixed with venous and arterial components
CI
compression bandages contraindicated if arterial component - hence imp of checking ABPI prior to treating any ulcer
types of gangrene
surgical options
dry - ischaemic necrosis
wet - infection plus ischaemia
50% of cases in diabetics
surg options
mid-tarsal amputation with femoro-distal graft
below knee amputation
the diabetic foot
large and small vessel disease
peripheral neuropathy leads to injury
‘loss of protective sensation’
tissue reperfusion injury
toxic factors - free radicals, histamine etc damage endothelial cells
the caps leak protein rich fluid into the muscles, which then swell and increase pressure within compartment
leads to vicious cycle as the swelling causes reduced venous return and cap perfusion leading to tissue hypoxia and further damage
initially leg is warm and arterial pulses are retained
similar events can occur with soft tissue trauma (crush unjury) and with fractures
nerve necrosis = painful hyperasthesiae then loss of sensation, motor loss eg foot drop
muscle necrosis = pain out of prop to injury, pain on passive movement of muscle, tense tender muscle on palp, rhado and AKI, later healing by fibrosis - volkmanns ischaemic contracture.
varicose veins what is it rf patho exam ix mgmt
what is it
dilated subcut vein with reversed blood flow
5% develop venous ulcer
rf FH preg obesity occupation
patho
NORMAL
1. blood flows normally from distal to proximal, retrograde flow in superficial veins is prevented by valves
2. blood flows from superficial to deep, additional valves in perforating veins ensure one-way flow and protect superficial veins from high pressure
3. blood in deep veins returns to heart aided by pressure generated by calf muscle pump
VARICOSE
1. primary valve prob in perfs = incompetent
2. high pressure from calf muscle pump transmitted outwards
3. superficial venous hypertension
4. varicose veins
5. progressive descending incompetence
POST THROMBOTIC LIMB
1. add in to above prev DVT, damages deep vein valves + deep venous hypertension
2. more likely to develop - lipodermatoscelerosis, venous ulceration, ‘post thrombotic limb’
exam
CEAP classification
c1 = thread veins
c2 = varicose
c3 = oedema
c4a = pigmentation and or eczema
4b = lipodermatosclerosis
c5 = healed ulcer ‘atrophie blanche’
c6 = active ulcer
inspect + palps
assess level of perf vein incompetence:
1. sapheno-femoral junct - extensive varicose veins over medial calf/thigh, sometimes saphena varix
2. mid-thigh perf - hunters vein - varicose over medial calf
3. small sapheno-popliteal junction - varicose over lateral calf
4. medial calf perfs - cocketts veins - varicose over medial calf
ix
duplex uss
tourniquet test - empty varicose by patient lying and raising leg, apply tourniquet high in thigh, ask patient to stand, veins below tourniquet fill and implies incomp perfs below that level, if remain empty then = above that level
mgmt
foam sclerotherapy
endothermal ablation (laser or radiofreq)
surgery - high tie and strip - trendelenberg procedure
chronic venous hypertension
damages subcut fat which become fibrotic = lipodermatosclerosis
skin around ankle feels hard and is tethered to subcut tissue
‘inverted champagne bottle’ leg
commonly assoc with deep vein reflux
what factors does warfarin inhibit
IX, X, VII and prothrombin II
9, 10, 12
what factors does rivaroxaban inhibit
Xa
what factors does heparin/ fondaparinux ACTIVATE
AntiThrombinIII
