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
