Cardiology/vascular Flashcards
turbulent flow
reynold’s number = (velocity x diameter x viscosity)/density; critical value is Re = 2000 for laminar, >3000 for mostly turbulent but smaller when velocity and tube diameter variable; turbulence causes breakdown in Darcy’s law so flow prop to sqrt of pressure as KE dissipated by disruptive forces due to inertial momentum; mainly in ventricles and aorta (diameter large), and where atheroslcerotic plaques have built up; vortex formation in turbulent flow establishes murmurs, seen in valve problems or stenosis of vessels due to atherosclerosis
CCP, laplace’s law and implications
CCP depends on vascular tone, with small tone it’s ~10mmHg; above CCP small arteries behave like rigid tubes
laplace law is wall tension = (transmural pressure x radius)/(wall thickness x2)
implications: if pressure is the same everywhere (it is), then as radius increases tension in wall increases; thus in an aneurysm, as it expands the tension in wall increases until it bursts; increasing the wall thickness could protect against this, but aneurysm is in an area of weakness/thinning; expansion can ease as becomes more spherical and better distributes pressure but this is more minor factor
second implication: LV pressure up (due to aortic stenosis, systemic HTN etc) means wall tension/stress up, so hypertrophy in response; meanwhile if chamber dilates (due to AR/MR, dilated cardiomyopathy, infarct) then tension/wall stress also increases, unless hypertrophy occurs
note laplace’s law is simplification when talking about heart, actual situation more complex but it’s a good basic explanation
ANS transmitters/receptors
NA mainly on alpha, adrenaline mainly on beta; alpha1 is vasoconstrictor, alpha2 presynaptic and control NA release; beta1 heart, beta2 bronchi and smooth muscle; pergang to postgang same for both Ach to nicotinic; then postgang to target for symp is NA to alpha/beta adrenergic; parasymp is Ach to nictotinic/muscarinic
exceptions eg ACh symp for sweat glands; ENS uses serotonin, dopamine and range of neuropeptides inc VIP
why regulate CO, why heart doesn’t set max, HR vs CO graph
must be regulated to ensure adequate tissue perfusion so eg inc in exercise, also important in ABP control; guyton et al replace dog heart with pump, CO plot against pump capacity: at normal or above no increase in CO, decrease does decrease, heart is necessary to maintain CO but doesn’t limit it; can’t raise CO on its own as circulation closed system, so reduces CVP to raise ABP by moving blood volume, but if CVP<1-2 below atmos then vessels collapse so heart can drive Pa-Pv gradient as far as CVP neg as any further and veins collapse, limiting VR/CO
HR inc inc’s CO up to a point, then CO drops as HR keeps increasing
what raises CO in experi’s, what is MSFP/what governs it, stressed vol etc
raising mean pressure in whole system (by increasing circulating volume or stimulating cat splanchnic nerve to promote venoconstriction) shown experimentally to raise CO; MSFP is mean pressure in circulatory system ie pressure that would be reached if heart stopped pumping; can be raised by raising volume (drinking isotonic fluid, transfusion) or constricting the volume, especially in veins as hold 2/3 of blood; 80% blood volume causes no pressure as doesn’t stretch walls, last 20% (stressed volume) causes MSFP to rise to ~7-10mmHg
why pressure greater in arts than veins - 2 reasons
transfer of blood volume changes pressures according to compliance, veins very compliant (10x more than arteries but stiff if overstretched) so reduction in pressure small here, less compliant arteries have greater increase in pressure, thus arteries more filled and veins less filled than they would be if heart stopped; arteriovenous P gradient then drives flow; veins collapse if CVP negative so MSFP sets max arteriovenous pressure gradient; heart cannot change mean pressure and MSFP determines max CO
CO equation, and controlling CO and MSFP (preload and afterload (inc how raised afterload incs end sys pressure), starling mechanism, HR and CO/RAP link + TPR/MSFP interactions and how much blood volume loss needed for MSFP to hit 0)
CO=(ABP-RAP)/TPR, (ABP-RAP) created by heart but limited by MSFP; TPR mainly influenced by arteriolar resistance
preload: initial stretching of the cardiac myocytes prior to contraction; increased by larger venous return, reduced heart rate (greater filling time), increased atrial contraction, and increased afterload (giving larger end sys volume); MR/TR stenosis decs preload on ventricles
afterload: increased by HTN, outflow valve stenosis (AS/PS), and dilation of the chamber (due to laplace’s law meaning more stress in the wall - likewise hypertrophy of chamber reduces afterload); an increase in afterload decreases the velocity of fiber shortening. Because the period of time available for ejection is finite, a decrease in fiber shortening velocity reduces the rate of volume ejection so that more blood is left within the ventricle at the end of systole, so makes starling mechanism less effective giving less SV and higher end sys pressure
starling mechanism: raised preload raises SV, up to a point; afterload and inotropic changes in contractility shift the curve
HR alone reduces SV, barely changes CO but facilitates increase in CO by steepening curve of CO vs RAP in exercise ie allows heart to change CO to lower RAP more effectively
increasing blood volume by 20% doubles MSFP as stressed volume doubled, reducing circulating volume by 20% would take MSFP to zero but symp venoconstriction can up to treble MSFP, reduces vessel volume to maintain MSFP above 0 until 40-50% of blood volume lost; as arterioles primary determinant of TPR, venoconstriction has little effect, and changes in TPR have little effect on MSFP as only 1% blood volume in arterioles
preload, afterload, and contractility - definitions and determinants (7 for pre, 4 for after, 8 for contract)
Preload can be defined as:
Myocardial sarcomere length just prior to contraction, for which the best approximation is end-diastolic volume
Tension on the myocardial sarcomeres just prior to contraction, for which the best approximation is end-diastolic pressure
The determinants of preload, if we choose to define it as a a volume, are:
Pressure filling the ventricle (intrathoracic pressure, atrial pressure, mean systemic filling pressure, cardiac output)
Compliance of the ventricle (compliance of pericardium, wall thickness, end sys volume of ventricle aka afterload)
Afterload can be defined as the resistance to ventricular ejection - the “load” that the heart must eject blood against. It consists of two main sets of determinant factors:
Myocardial wall stress, which represents intracardiac factors
Input impedance, which represents extracardiac factors
wall stress determined by Laplace law, input impedance incs arterial stiffness, LVOT resistance (raised in HOCM/aortic stenosis), arterial resistance (inc blood viscosity and vessel radius)
Contractility is the change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume)
Increasing preload increases the force of contraction (frank-starling)
Afterload (the Anrep effect)(The increased afterload causes an increased end-systolic volume which increases the sarcomere stretch)
Heart rate (the Bowditch effect) (With higher hear rates, the myocardium does not have time to expel intracellular calcium, so it accumulates, increasing the force of contraction)
also dependent on extracellular Ca level, catecholamine conc, ATP level (O2, phosphate), temperature, pH
venous return
VR = (MSFP-RAP)/RvR; negative RAP only helps so far, too negative and veins collapses
RvR reflects eg work done against gravity t get blood from feet to heart; RVR can change (eg exercise and muscle pumps) but isn’t regulated
CO in heart disease and shock (if MSFP up but heart cant raise CO)
if heart cannot increase CO but MSFP rises then RAP rises leading to increased Pc and oedema; body continues to attempt to raise CO but can’t giving heart failure; if CO inadequate to perfuse tissues then shock: hypotension, tachycardia with low urine output, loss of consciousness; loss of volume (hypovolaemic - low ABP with low RAP) or cardiac pathology (cardiogenic - low ABP with high RAP - may see narrow pulse pressure with lower sysBP and higher diastolic); distributive shock (CO may be normal or above normal, abnormal blood distribution in small vessels, tend to see a wider oulse pressure) due to fall in vascular tone or extravasation of plasma decreasing MSFP caused by septicaemia, anaphylaxis or failure of symp innervation if eg spinal cord severed; obstructive shock (eg tamponade) similar to cardiogenic - hence narrow pulse pressure post CABG or other heart op should make you consider tamponade or need for inotropes
blood pressure estimation with palpation
pulse strength is proportional to pulse pressure not MAP/sysBP, which is why AR pt has bounding pulse; distributive shock bp 70/30 will have stronger pulse than cardiogenic shock 105/80, and if you have LVAD may have no pulse at all
however as BP falls pulses are lost reliably in order radial -> femoral -> carotid
grade I-IV hypovolaemic shock and estimating blood loss volume per ATLS
clinical symptoms of volume loss in class I patients (estimated blood loss up to 15%) are minimal. No measurable changes occur in systolic blood pressure (SBP) or mental status and only a mild tachycardia (<100 beats/min) may be observed. In class II (estimated blood loss 15–30%) a tachycardia of >100 beats/min may be present and subtle changes in mental status, e.g. anxiety, are described. In contrast, SBP is still within normal limits. As blood loss increases to 30–40% (class III), a marked tachycardia (120–140 beats/min), a measurable hypotension and an impaired mental status may occur. A further depletion of blood volume (>40%) is characterised by a significant hypotension, a tachycardia of >140 beats/min and a markedly depressed mental status, which may further proceed into a complete loss of consciousness
however note that this is only a rough guide and various studies have shown flaws with it - go off other things too; base deficit can be used to predict transfusion requirement and mortality - larger base deficit being worse
baroceptors and chemoreceptors (inc short and long term sensors and controls, feed-forward and putting it all together)
at carotid baroreceptors, aortic arch and afferent arterioles, stretch sensitive nerve endings meshed with elastic lamellae in regions with relatively little collagen and smooth muscle so stretch triggers increase in activity to stimulate neurons in NTS and inhibit the vasomotor centre; carotid more sensitive than aortic arch, aortic arch can sense higher ABP values that saturate the carotid response, so wide range achieved; carotid of dog B attached to circulation of dog A, adrenaline into dog A increasing its blood pressure and giving reflex fall in blood pressure in dog B - Heymans experiment; denervation means ABP more variable but mABP roughly constant - less responsive to eg postural changes or activity (high pressure control short term); high pressure reset to higher ABP if mABP increases
carotid, aortic bodies and medulla, mainly control ventilation and not important to ABP control normally; when very low or pO2 significantly reduced then do have a role, important as high pressure baroreceptors relatively unresponsive under severe hypotension; aortic/carotid detect low O2 delivery and medulla high pCO2
low pressure baroreceptors: neither of the other control systems affects mABP; as MSFP important in ABP, stretch receptors in low pressure areas: atrial-venous junctions and inside atria: cardiopulmonary baroreceptors; essentially detect RAP as if it’s raised, suggests heart not maintaining low venous pressures, if low suggest heart CO high enough; denervation gives rise in mABP; firing rate increases with pressure to NTS then hypothalamus to influence ADH secretion, symp activity (esp renal nerve), thirst and Na appetite; reduced pressure gives ECF vol increase, raising circulating vol/MSFP
exercise, standing up etc don’t cause detectable mABP drop, suggesting feed-forward mechanism; pain/anger/fear raise mABP in preparation for fight/flight; cortex, joints and cerebellum to medulla if exercise initiated; cardiovascular control centre in medulla gets input from feed-forward, baro/chemoreceptors; medulla integrates then generates appropriate response via symp and PS
symp, parasymp, and ABP - inc distribution of bloodflow and tonic activity, and broad challenges to ABP maintenance in healthy person
postgang along blood vessels to give vaso/venoconstriction by NA on alpha1 adrenceptors; raises TPR/MSFP; also redistributes bloodflow: heart/brain get greater proportion as relatively little vasoconstrictor innervation
vasoconstrictor nerves tonically active (1-4Hz) with activity able to increase to 10Hz which can cut off blood supply to some tissues in eg H+; resting tone allows inhibition to reduce ABP and means that damage above eg T1 leads to rapid ABP drop and shock; also innervate heart (SAN, atria, ventricles) to raise contractility and HR, have a low resting frequency
chromaffin cells, adrenaline release, alpha1 constriction; but also beta2 dilation in coronary arteries, skeletal muscles, NA acts on alpha1 at skeletal to restrict if necessary
PS on SAN, AVN, conducting system; slows heart rate by slowing conduction; shows tonic activity (rare PS example) and inhibition of this by eg atropine shows dramatic increase in HR; M3 muscarinic receptors in endothelium do the NO vasodilation thing
challenges to ABP as local blood flow increases needed for eg digestion, exercise, thinking etc which necessitates local vasodilation which could give fall in TPR (5 or 6 fold in full body exercise) yet mABP relatively constant; CO must increase and skin/muscle/GIT can have symp vasoconstriction to divert blood; must raise MSFP then HR/contractility to ensure raised MSFP raises CO and not just RAP; this is all short term, long term is based on ECF volume (renal stuff)
functional hyperaemia
2 phased, rapid increase of blood flow; phase 1 is 2 to 15-20 secs after starting exercise, with rapid increase, and after ~20 seconds slow increase to sustained max flow in phase 2, can be seen on blood flow (ml per min) against time (min) graph
most local changes too slow to explain this fast change; muscle APs produce immediate and fast increase in IF [K+] to as much as 10mM; this hyperpolarises the arteriolar smooth muscle to close VG Ca channels and relax the muscle; hyperpolarization due to enhanced Na pump activity and enhanced inwardly rectifying K channels, blocking either channel (ouabain or barium respectively) attenuates vasodilation by ~60%; second fast cause is muscle pump raising VR which not only enhances CO but also reduces local venous pressures to increase pressure gradient through muscle caps; neurogenic vasodilation eg symp fibres in cats plays role, probably doesn’t occur in humans
hard to investigate as multiple redundancies meaning isolating one system leads to compensation by others; circulating adrenaline on beta2 has an effect as does continued raised [K]if; reduced pO2 unlikely to have an effect as not shown to reduce in vicinity of arteriole smooth muscle; does give raised O2 offloading by Hb giving ATP/NO release from RBCs, low pO2 enhances activity of ectonucleotidases which make adenosine from ATP, then serving as a vasodilator; ATP from active muscle turned into adenosine too, some relase via CFTR channels in response to reduced intracellular pH (which occurs in exercise eg lactate); adenosine acts on A2a receptors to raise cAMP levels, activating PKA to open K channels to hyperpolarise the membrane, acting synergistically with already raised [K]if
systemic response to functional hyperaemia (inc what happens to pulse pressure)
venoconstriction, reduced vagal tone to heart, increased symp to heart; muscle pump assists, can be considered to reduce RVR, probably ‘halving’ it as MSFP up 3x but CO up 5-6x; feedforward responses feed in to medulla to mediate this and from brao/chemoreceptors; using curare to block NMJ allows separation of command to exercise from exercise to observe significane of feed-forward response: HR may increase without exercise, or before it begins; baroreceptors reset to a new set point and maintain the higher ABP during exercise, possibly due to impulses from joint receptors to NTS, the raised mABP shows feedback control isn’t primary response; pulse pressure widens reflecting increases contractility and decreased TPR
limiting factors in exercise
O2 uptake not usually limiting: raising inhaled pO2 doesn’t significantly improve performance; nor is muscle’s ability to work: power output pedalling with two legs not double pedalling with one suggesting two legs don’t reach max power output; unfit people may not have aerobic capacity to demonstrate this effect in which case their own muscles are limiting; suggests circulation is limiting even though not possible to exercise so hard that ABP drops, suggesting central control of activity levels; fatigue relates to circulatory capacity; reduced CO thus reduces exercise performance/gives fatigue
O2 delivery and extraction
VO2 = Oxygen consumption is the total amount of oxygen removed from the blood due to tissue oxidative metabolism per minute
DO2 = Global oxygen delivery
O2 ER is the oxygen extraction ratio
VO2 = DO2 x O2 ER
Paediatric DO2 range from 160 to 804ml/min2
and oxygen consumption index values range from 120 to 200ml/m2. O2ER is 25% and varies for different organs. Oxygen that is not extracted returns to the mixed venous circulation. A Scv02 (central venous
oxygenation saturation) of 70% indicates oxygen delivery is adequate.
At ‘critical DO2’ however, the maximum O2ER is reached. Beyond this point, any further increase in VO2 or decline in DO2 leads to tissue hypoxia and anaerobic metabolism
DO2 = CO x CaO2 (CaO2 = (Hb x SaO2 x 1.34) + (0.003 x PaO2))
reduced O2 delivery: Hypoxia, anaemia, poor contractility, shock, abnormal heart rate
or rhythm
increased O2 consumption: Fever and inflammatory states eg sepsis, burns, trauma, increased metabolic rate, increased muscular activity, increased respiratory effort
impaired O2 extraction/use: Sepsis, cyanide poisoning
Stroke Volume (SV) is a function of preload, afterload, contractility and diastolic relaxation. Therefore optimising heart rate (HR), contractility, diastolic relaxation, preload and afterload improves cardiac output (CO).
* Oxygen carrying capacity can be increased by raising haemoglobin and optimising its saturation with oxygen.
* Systemic oxygen delivery can be improved by manipulation of all these factors.
* A reduction in oxygen consumption can be achieved in a number of ways, including intubation and ventilation, sedation and temperature control.
circulatory physiology in haemorrhage (inc autotransfuse vol and how long to restore haematocrit)
response to reduced volume and pain/emotional state; vol down so MSFP down so VR down so CO down; baroreceptors detect and relieve inhibition on medullay vasomotor sensors which may be stimulated by eg hypothalamus as response to fear; vagal tone to heart down, symp gives raised tone/HR; catecholamines, Ang2 and ADH released with vasocontrictory and water retention effects; smooth muscle contracts when stretch reduced, autotransfusion of 500ml-1L; long term (tens of minutes) renal conservation of fluid, thirst and Na appetite helps restore balance; 24-48 hrs later plasma proteins replaced by liver and 3-4 weeks later haematocrit is restored, stimulated by erythropoietin from kidneys in response to reduced O2 delivery
cardio responses to hypoxia
2 different responses due to either lack of O2 as can’t breathe (diving) or lack of O2 as less in air (ascent to altitude); first form O2 conserved for brain, 2nd CO increased to make up for lowered pO2; reflex response to low pO2 is slowed HR and vasoconstriction by vagus and symp systems respectively, called diving reflex(or primary chemoreceptor response, reduces heart work to minimum and overrides local vasodilation due to decreased pO2 so more for brain; secondary chemoreceptor response if reduced pO2 increases rate/depth of breathing (as it does if breathing not restricted) so pulmonary stretch receptors to vasomotor centre of medulla giving venoconstriction, increased HR and vasodilation/constriction pattern that favours vital tissues giving CO rise: animal studies of sleep apnea suggests chronic hypoxia gives chronic hypertension this way
catecholamines and the heart (inc signal pathway for beta1 and M2 and how that leads to effects)
mediated by cAMP with beta1 on nodal and ventricular cells and muscarinic M2 confined to nodes mainly; beta1 coupled to Gs, giving rise in cAMP and not only modulates pacemaker potential but also enhances Ca entry into cells; patch clamp experiments show effect of cAMP on L-type channels, increasing the likelihood of their opening; time course for stim of I-CA is slow with latent period of ~5s and ~30s for max I to be reached; this due to cAMP must be produced, PKA activated then phospho the channel and reversal also slow
Ryr sensitised so more Ca-dependent Ca release which in addition to increased Ca entry via L-type channels gives inc force of contraction: positive inotropic effect; PKA phospho’s SERCA/phospholamban to help clear Ca; If potential at which activates shifted more positive so pacemaker produces more frequent APs - positive chronotropic; delayed rectifier currents enhanced giving shortened AP duration: positive chronotropic
Ach - cAMP formation inhibited by M2 coupled through Gi/o, undue activation by eg excessive vagal stim can even stop the heart; I-Ca reduced giving negative chronotropic effect but not negative inotropic as M2 largely confined to nodal cells so not much influence on ventricles; negative shift in activation pot for If meaning pacemaker produces more widely spaced APs: negative chronotropic; IK-ACh current stimulated which hyperpolarises cell so more difficult to elicit APs
myocardial contractility and inotropes - what impairs (5 things one a drug), when vasopressors indicated (how admin, risk to heart), examples of this and inotropes
contractility can be impaired by hypoxaemia, hypocalcaemia, hypophosphataemia, b blockers, severe metabolic acidosis
if signs of shock despite adequate fluid replacement and organ perfusion at risk then vasopressor therapy; heart O2 demand inc’d by this with risk of ischaema and so be careful, esp in cardiogenic shock after MI; vasopressors are administered via central vein and continually monitored
egs inc adrenaline (low dose beta effect dominates, high dose alpha inc vasocontriction which long term has risk of gangrene and lactic acidosis), noradrenaline mostly alpha so useful if vasodilated eg septic shock; can be used alongside dobutamine (beta1) to optimise CO; noradr can be further supplemented with vasopressin
phosphodiesterase inhibitors like milrinone bypass beta receptors so no tachycardia, just pos inotropy, thus good if heart failure, on beta blockers, receptors downreg’d etc
dobutamine good if cardiogenic shock
starling curve axes, improving SV (inc 2 ways of shifting along the curve, how to shift whole curve down/right or up/left x2, and a summary of approaches x3 to improving CO), 3 good consequences of reducing afterload + condition where esp good, 2 drugs that do this, and when to be cautious; if inotropes aren’t working then what x2
frank starling curve SV vs preload
diuresis moves left along the curve, fluid bolus moves right along the curve; increasing afterload or reducing contractility shifts curve down and to the right (ie smaller SV for a given preload), and vice versa;
thus in general to improve BP we want to improve CO, to improve CO we want to improve SV not HR (*unless pt bradycardic), and to improve SV we want to shift along the curve (fluids, diuresis) or improve contractility or reduce afterload (though in practice we increase afterload aka TPR to raise mABP, thus focusing on contractility)
can reduce afterload and thus inc SV and decease myocardial O2 demands, and reduce wall tension of myocardium; good if heart failure, esp if ventricular function poor; eg sodium nitroprusside, nitroglycerine, but caution if hypotension
if inotropes arent working then eg mechanical support of myocardium eg intraaortic balloon counterpulsation; ventricular assist devices also
mean arterial pressure targets (inc what if aiming too low or too high, how to calculate)
general target is 65mmHg but can be individualised as optimal may be higher in older ppl with atherosclerosis or HTN that they’ve adapted to etc than younger pts - eg up to 75mmHg or so, maybe even 85mmHg if chronic HTN
if too low hypoperfusion, if too high then vasoconstriction can lead to ischaemic injury, AKI etc
to calculate: diastolic pressure + 1/3 of the pulse pressure
causes and assessment of hypotension: 3 common causes, general initial assessment: SV vs HR, ddx 4:8:8:9:1, 7ix/things to check (10 bloods)
common causes: dehydration, bleeding, medications
is SV or HR too low? if HR low, then positive chronotropes; if SV too low then assess fluid responsiveness with a bolus (need to measure BP before and afterwards) -> if fluid responsive then give a larger bag of fluids as volume down; if not responsive then contractility down so give inotropes; in both of these latter kinds pressors may be needed to support the BP
dd
preload down due to true volume depletion (bleed, dehydration, polyuria, fluid sequestration) or impaired venous return (PEEP, tension PTX, constrictive pericarditis, PE or pulm HTN, tamponade, caval compression by pregnancy tumour etc, valve disease)
afterload down due to SIRS, sepsis, anaphylaxis, spinal shock, hypothyroid, liver failure, adrenal insufficiency, medications)
contractility down due to MI, dysrhythmia, heart failure, hypothermia, hypophos, hypothyroid, hypocalcemia, acid/alkalosis, LA toxicity
HR down due to the many causes of bradycardia
so ix: assess fluid responsiveness with bolus and BP before and after; check urine output and examine for sources of bleeding or infection or signs of above pathologies; check medications (inc what they normally take in case something missed); ECG; bloods to inc CRP, U&Es, bone profile, mg, LFTs, TFTs, NT-pro-BNP +/- d-dimer, trop, 9am cortisol), ECHO if indicated from previous tests
5 cannula colours and their flow rates
Orange 14g 270ml/min
Grey 16g 180ml/min
Green 18g 80ml/min
Pink 20g 54ml/min
Blue 22g 33ml/min
heart failure intro (inc pumping range of normal heart, main problems in right and left HF, what exacerbates fluid situation, overall aims of drug therapy)
results from heart failing to maintain adequate circulation; tissues regulate their own bloodflow according to metabolic needs, and heart then adapts to loads placed on it, with a healthy heart able to pump from 2-25L per min; if heart doesn’t operate properly then more blood returns than it can deal with, causing increased filling pressure and congestion of venous circulation; veins are distensible so can accommodate a lot of blood but inc Pc causes oedema; right side failure causes peripheral oedema (ankles, fingers, etc) and left side gives pulmonary oedema which compromises oxygenation of blood, potentially making the heart failure worse; this occurs in cardiogenic shock and is a very serious condition; undeperfusion of kidneys causes renin secretion which leads to fluid retention and exacerbates the situation; right or left sided failure tend to cause breathlessness, cyanosis and fatigue; drug treatment based on increasing ventricular contractile force and reducing MSFP to reduce load on heart; diuretics and ACEi/ARBs important; isosorbide dinitrate/hydralazine can be used to reduce preload/afterload in certain populations eg african americans (respond less to ACEi); tolvaptan (ADH antag)) inc Na output so urine output
heart failure (inc what exacerbates (7 things), what may mimic), sx, classification, initial ix
acute due to MI, arrhythmia (AF), acute valve dysfunction and gives acute dyspnoea and pulmonary oedema
chronic also occurs
70% due to IHD. also idiopathic dilated cardiomyopathy, valve disease, hypertension, connective tissue disease, infections, beri-beri, haemochromatosis,
may be exacerbated by arrhythmia, MI, anaemia, reduction in therapy (by self or doctor), infection, PE, alcohol
beware eg hypoalbuminaemia, drug induced fluid retention, chest or lung disease, renal/hepatic disease, and others may mimic
fatigue, dysponoea, orthopnoea, PND, peripheral oedema, chest pain, palpitations, hypotension, rJVP, displaced apex beat, gallop rhythm, cachexia
multisystem eg hepatomegaly, ascites, reduced bowel perfusion, oliguria/anuria, confusion, insomnia, psychosis, anxiety, gout, carpal tunnel
class 1-4 (normal/exercise, exertion (like going upstairs) minimal exertion (getting dressed), symptoms at rest)
if suspect heart failure: try to exclude through 12 lead ecg, natriuretic peptides (pro-bnp <400ng/L makes HF less likely but levels can be high in PE, left vent hypertroph, hypoxaemia, sepsis, cirrhosis and COPD; send for echo in 2 wks if >2000, if 400-2000 then echo in 6 wks) consider: CXR, blood tests (most normal ones), peak flow or spirometry; if both first two normal then heart failure unlikely, if one or both off then do echocardiography (key investigation, mandatory to confirm it); go straight to the echo if clear history suggesting heart failure and a reason for it eg past MI or many risk factors
managing heart failure
loop diuretic for all
reduced systolic function on the echo: ACEi (or ARB), beta blocker (note only bisoprolol, metoprolol, carvedilol have evidence for improved mortality in HF); if symptoms/signs dont persists and LVEF >35% then leave; if LVEF<35% consider ICD
if those 3 dont get rid of symptoms/signs then add aldosterone antag + SGLT2i and if cant then ARB on top of ACEi; if no more persisting symptoms look at the LVEF as above; if there are then is QRS >120ms; if no then ivabradine/digoxin/hydralazine/nitrates and if yes then CRT-P/D; refer for LVAD, transplant, palliative care if nothing even after that
diagnosing and classifying chronic heart failure (stage A-C and other classification system), what if uncertain diagnosis esp of eg HFpEF, and what diastolic dysfunction means
Stage A are pts at risk, and need primary prevention by controlling risk factors like HTN, DM, genetic screening etc; can screen with NT-pro BNP and multivariate risk scores
Stage B are pre-HF and can have BB and ACEi; if LVEF <50% shouldn’t use thiazolidinediones or non-DHP CCBs
diagnosis of stage C (HF) and stage D (advanced HF) as per other cards, classify into rEF if <40%, pEF if >50%, and impaired EF if 40-50
also classify with NYHA
Exercise stress testing with echocardiographic evaluation of diastolic parameters can be helpful if the diagnosis remains uncertain, and also for functional assessment in later stages of mx eg for surgery planning
LV filling is composed of passive and active filling. Passive filling occurs as the mitral valve opens and blood is sucked into the LV as the chamber relaxes….this relaxation is impaired by things that damage the myocardium such as HTN, ischemia, etc. Active filling occurs at the end of diastole as the atria contracts to complete LV filling. A higher proportion of LV filling occurs during this active phase when patients have grade 1 diastolic dysfunction. This is clinically important because stiff ventricles do not respond favourably to extra volume, and these patients do much better in NSR because of their reliance on organized atrial contractions to fill the LV
passive filling is E, active filling is A. E/A ratio is the major determinant of DD, with different patterns corresponding to grade of DD
detailed heart failure mx (HFrEF) (lifestyle, medications - inc when not to give MRAs and ARNI type drugs, devices, what to avoid - 4 drugs)
avoid excessive sodium, with dietician support to avoid also getting eg micronut deficiencies
exercise training also good
loop diuretic for sx relief if retaining fluid, and can add thiazide if not responding to high dose loop (ie go up on loop dose first)
HFrEF and NYHA 2+ start ARNI, or switch ACEi or ARB to ARNI; use one of these other agents if ARNI not tolerated; important to let ACEi wash out before starting ARNI due to oedema risk - need to wait 36 hours after last ACEi dose; any history of angioedema then no ARNI and no ACEi
HFrEF with current or prev sx start bisoprolol, carvedilol, or sustained release metoprolol (others not recommended by AHA)
if HFrEF and NYHA class 2+ can add eplerenone (men) or spironolactone (anyone) if eGFR >30 and K <5, discontinue if K raises >5.5 while on MRA
in HFrEF with sx add dapagliflozin
if symptomatic HFrEF including BB at max tolerated dose and in SR with HR >70bpm then you can add ivabradine
IVD and CRT can be considered as in above flashcards
you should avoid nonDHP CCBs, thiazolidineodiones, DPP4 inhibitors, NSAIDs
detailed heart failure mx (HFimpEF and HFpEF) amyloidosis(4ix + cMRI finding)
impaired: diuretics as needed, SGLT2i, ARNI etc, MRA, BB
HFpEF: attain BP control, manage AF, SGLT2i, MRAs, ARNI/ARB
amyloidosis: serum and urine monoclonal light chains, bone scintigraphy if no light chains, then if confirmed either way genetic testing for TTR gene; will see late gadolinium enhancement on cMRI;
heart failure timescale for echo, lifestyle/non-medical mx x4
suspect, check NT-proBNP, if >2000 then urgent echo, if 400-2000 then echo in 2 weeks (can be OP), if <400 HF unlikely
Stop smoking and alcohol, reduce salt, lose weight, get vaccination for flu and pneumococcus.
pulsus alternans - general cause and 7 specifics, 2 hypotheses for causes
due to ventricle strain esp LV sys impairment - left if heart failure, CAD, AS, cardiomyopathy and right in PE or pHTN
may also be linked to pericardial effusion but has different aetiology to electrical alternans
may result from abnormal ca handling or frank-starling (poor EF so raised EDV meaning next preload is larger giving bigger SV and smaller EDV then repeats); both are just hypotheses
acute heart failure (ward based scenario, 2 things to first exclude, then 6 acute causes to look for; 4 mx steps inc furo dosing and 2 things showing response, BP guides for other steps); 4x and 2 things to monitor; when stabilised mx x3, if worsening steps x3 and what may need to be managed as if BP keeps dropping (what to stop in this case); 3 abx combo options for IE, surgery x2 reasons
When you are on the wards and a nurse asks you to review a patient that has just started desaturating ask yourself how much fluid that patient has been given and whether they might not be able to process that much. For example, an 85 year old lady with chronic kidney disease and aortic stenosis is prescribed 2 litres of fluid over 4 hours and then starts to drop her oxygen saturations. This is a common scenario and a dose of IV furosemide can often work like magic to clear some fluid and ease their breathing
first exclude cardiogenic shock, then is there resp failure requiring CPAP/BiPAP or ventilation? if no is there an acute cause (ACS, HTN emergency, arrhythmia - AF, valve disease, aortic dissection, PE), if obvious cause treat that while managing the acute heart failure
Acute heart failure management:
Sit your patient upright
Start high flow oxygen/CPAP if needed
Start slow IV furosemide (40mg IV repeating every 60 mins up to 240mg total if pt not had loop diuretics before, if they have then 80mg repeating every 60 mins to 240mg max - an alternative would be an infusion) - response is breathlessness reducing and diuresis >30ml/hr)
if BP is over 90mmHg consider GTN spray, if not responding to diuresis can do GTN or long acting nitrate infusion as long as BP remains >90mmHg and if sysBP >100mmHg can do IV morphine 2.5-10mg too (generally don’t unless severe breathlessness)
Do an ECG, get IV access and draw bloods, monitor vitals along with urine output, get ABG and CXR
If your patient stabilised give oral diuretics if not on, go back to chronic management; review every hr to check they don’t need more diuretic IV
If patient is worsening, give further IV furosemide, start CPAP and if BP dropping transfer to ITU. Most importantly CALL YOUR REG!! and be aware that this may need to be managed as cardiogenic shock if sx of shock develop (eg BP <85mmHg) - make sure you stop all vasodilators in this case
note 40 mg furosemide PO = 1 mg bumetanide PO
IE first time is amox + gent, vanc and gent if sepsis or embolic features, add rifampicin if prosthetic valve
change once you have culture results
surgery if heart failure resistant to medical therapy, severe valve problems
management of cardiogenic shock (also pathophys and 16 causes, 11ix)
Acute deterioration in the left ventricular (LV) contractility is usually the main cause of CS. However, impaired right ventricular (RV) systolic function and deranged vasculature functionality may also contribute/cause
Hypoperfusion of vital organs triggers catecholamine and vasopressin release, aiming to improve end‐organ perfusion by augmenting myocardial contractility and peripheral vasoconstriction. In the short‐term, such neurohormonal changes improve tissue perfusion. However, persistently elevated levels have a detrimental effect on myocardial function due to elevated afterload and myocardial oxygen demand
acute MI big cause, but also consider myocarditis, takotsubo, HOCM with outflow obstruction, decompensation of cardiomyopathy of any kind, septic cardiomyopathy, bradycardia/AF/VT/VF, tamponade, constrictive pericarditis, thyroid disease, valvular disease (acute MR, bad AS/MS), free wall rupture, aortic dissection, PE, overdose of BB/CCBs, acidosis
get bloods (inc bone profile, Mg, phos, coag, TFTs, NT-pro BNP, trop), ABG, ECG, echo, CXR
most effective therapeutic intervention in patients with AMI complicated by CS (AMI‐CS) is establishment of coronary reperfusion, at the earliest possible. However, in the interim, their hemodynamic instability should be managed ensuring adequate oxygenation and ventilation, preservation of euvolemic state, and general critical care measures
manage with ACS treatment and:
O2, IV fluids, inotropes and vasopressors - noradrenaline best to use, others may inc adrenaline, vasopressin, isoprenaline (beta1/2 agonist); should put catheter in to monitor fluid balance; pt may need ventilatory report including intubation
percutaneous LVAD can also be used, and ECMO
guide to different inotropes(vaso constrictors vs inodilators/constrictors; choices for low HR (1 -> why it is good choice even in CHB), dilated vessels (2 options, if no central 5 options), pump failure (2), agent not used anymore and why, choice for rescue drug (3 problems with it)
vasoconstrictors (squeeze), inoconstrictors (push and squeeze), inodilators (push and relax)
select agent depending on which combo of above effects you want to achieve
Low heart rate use a chronotropic: Isoprenaline (isoprenaline as positive chronotropic effects that bypass the AVN meaning that it can be used to maintain HR as a bridge to formal pacing)
Low BP, work out why it’s low.
Hypovolemia: give volume - crystalloid or blood products.
Dilated vessels: vasopressors - noradrenaline is usually first line if there’s CVC access, add vasopressin if needing lots of norad. In no central access options are ephedrine ( also increases HR, metaraminol or phenylephrine ( both decrease HR - baroreceptor response to increased preload without pos chronotropic effect to counteract) -> generally these 3 are done by anaesthetists, or dilute peripheral norad (or you can either bolus dilute adr or even set up an adr infusion).
Pump failure: inotropes - milrinone, dobutamine
dopamine tends not to be used anymore due to being v arrhythmogenic and not superior in efficacy
adrenaline is generally used as a rescue drug and it does work well as an inoconstrictor, but it causes lactic acidosis and hypokalemia, as well as potentially hyperglycemia and pt may need insulin
acute onset heart failure workup (inc 2 main ix, 5 essential ix, 6 other ix, aetiology mnemonic inc 6 causes for the M)
if suspect then pro-BNP: if <300 then ruled out, if >300 is possible and can proceed to echo; alternatively if strong suspicion can go straight to echo
other you should do: ECG, trop, U&Es, ABG if unwell, CXR +/- lung US
others you could do: iron studies, TFTs, procalcitonin if pneumonia a dd, d-dimer if PE a diff, serum lactate, VBG
CHAMPIT: aCs, hypertensive emergency, arrhythmia (AF), mechanical cause, PE, infection/inflam, tamponade
mechanical causes - free wall rupture, VSD, acute MR, chest trauma, infective endocarditis, aortic dissection
4 presentations of acute heart failure and mx of each
acute decompensation: onset over days with fluid retention giving systemic congestion - loop diuretics, add another kind if resistant and/or increase dose to max, if diuretic resistant then consider RRT or palliative care; if hypoperfusion consider inotropes in addition to loop diuretics, if persistent hypoperfusion consider adding vasopressors, if still then mechanical support +/- RRT; also try to identify a precipitant with your workup, and treat that
acute pulmonary oedema: dyspnoea with orthopnoea, resp failure, tachypnoea; start high flow O2, escalate early to CPAP or BiPAP as required; IV diuretic; IV vasodilator (eg GTN) if sysBP >110mmHg, to reduce afterload (rarely may instead have low BP and hypoperfusion which should be managed stepwise as above), as above can consider RRT and MCS if needed
isolated RV failure: systemic congestion which may eventually reduced LV filling and so CO; if there PE or ACS? treat if so; if not, then fluid balance and input/output charts, if marked then consider diuretics; if hypoperfusion/persistent hypotension then stepwise support as above; if not working then RRT or RVAD
cardiogenic shock: managed as in other cards
in all of the above, if NIV failing can consider intubation
diuretics and vasodilators in acute heart failure - inc initial diuretic dose, 2 ways to assess for response and what to do if unsatisfactory, where nitrates vs nitroprusside act, GTN infusion)
High diuretic doses may cause greater neurohormonal activation and electrolyte abnormalities and are often associated with poorer outcomes - start a bit lower and build
initial i.v. dose of furosemide, or equivalent dose of bumetanide, corresponding to 1–2 times the daily oral dose taken by the patient before admission. If the patient was not on oral diuretics, a starting dose of 20–40 mg of furosemide is good
2–3 daily boluses or as a continuous infusion. Daily single bolus administrations are discouraged because of the possibility of post-dosing sodium retention
With continuous infusion, a loading dose may be used to achieve steady state earlier. Diuretic response should be evaluated shortly after start of diuretic therapy and may be assessed by performing a spot urine sodium content measurement after 2 or 6 h and/or by measuring the hourly urine output. A satisfactory diuretic response can be defined as a urine sodium content >50–70 mEq/L at 2 h and/or by a urine output >100–150 mL/h during the first 6 h; If there is an insufficient diuretic response, the loop diuretic i.v. dose can be doubled, with a further assessment of diuretic response; If the diuretic response remains inadequate, e.g. <100 mL hourly diuresis despite doubling loop diuretic dose, concomitant administration of other diuretics acting at different sites, namely thiazides or metolazone or acetazolamide, may be considered. However, this combination requires careful monitoring of serum electrolytes and renal function
IV vasodilators are nitreates or nitroprusside; Nitrates act mainly on peripheral veins whereas nitroprusside is more a balanced arterial and venous dilator; Nitrates are generally administered with an initial bolus followed by continuous infusion. However, they may also be given as repeated boluses. Nitroglycerine (aka glyceryl trinitrate) can be given as 1–2 mg boluses in severely hypertensive patients with acute pulmonary oedema; infusion rate 1 ml/hr, can build up to 3-5ml/hr or even higher (this is also the case when using it for pain or BP control - max in all cases is 12ml/hr); note GTN may cause headaches (v common, will pass - if from ISMN can try standard release smaller doses twice a day instead of MR once a day), hypotension
paediatric cardiogenic shock
cardiogenic shock is considered “pump failure”.
Myocardial dysfunction, usually systolic, is responsible for the failure of the cardiovascular system to meet the metabolic demands of the body
Common causes: myocarditis, cardiomyopathies, congenital disorders, valvular disease (sec to eg rheumatic fever)
Reduced myocardial contractility leads to a rightward shift of the left ventricular end-systolic pressure volume curve and a fall in stroke volume. A metabolic acidosis can develop which may impair contractility further. Hypotension may ensue, prompting a fall in
coronary perfusion pressure and subsequent myocardial ischaemia.
A rise in left ventricular end diastolic pressure (LVEDP) from diastolic dysfunction causes decreased myocardial perfusion pressure
and pulmonary oedema, contributing to hypoxemia and myocardial ischaemia. A downward spiral of failing myocardium and worsening myocardial ischaemia can be difficult to break and reverse. Significant
arterial oxygen desaturation often occurs in cardiogenic shock as a result of a decrease in mixed venous oxygen saturation (SVO2)
and intrapulmonary shunting. SVO2 decrease occurs as a result of increased tissue oxygen extraction because of the low CO.
Tachycardia is the main compensatory mechanism to maintain the CO and systemic
perfusion. Nonspecific signs of shock suggestive of poor perfusion include oliguria, cyanosis, cold extremities, weak distal pulses,
lethargy or altered mentation and hypotension. Signs of heart failure may give a hint to the cause being cardiogenic shock. These include
irregular pulse, narrow pulse pressure, hepatomegaly, distended jugular vein, heart murmur, gallop rhythm, distant heart sounds
and pulmonary crackles. Infants may present with difficulty feeding, while older children may complain of difficulty breathing and chest
pain
CXR usually diagnostic, also need ECG, blood gas, and bloods to inc FBC, U&Es, LFTs, bone profile, Mg, CRP, ASOT, pro-BNP, trop, CK, ANA, anti-dsDNA, ESR, consider viral serology
goals of management of a patient in cardiogenic shock are threefold:
1. Minimise oxygen demand/consumption
2. Maximise myocardial performance and systemic oxygen delivery
3. Treat underlying cause
will need serious support so liaise with PICU early
If able to maintain airway – give O2 with positive end expiratory pressure (PEEP) aim >92%
- PEEP has both advantages and disadvantages in cardiogenic shock. Not only can it increase airway pressure and improve oxygenation and alveolar recruitment, but also decrease left ventricular afterload due to decreased LV transmural pressure.
However, PEEP can lead to decreased cardiac output through its effects on the right heart (decreased RV preload and increased RV afterload)
If apnoeic or unstable airway – plan early intubation using ketamine and rocuronium
- If patient requires intubation, this is a very high-risk situation (possibly commence inotropes before intubation, use ketamine as least cardio-depressant, and prepare for possible arrest in advance)
Obtain IV access.
- Assessment of fluid status: optimise preload
- If evidence of dehydration use volume expansion with small fluid boluses (5-10mL/kg)
- If evidence of fluid overload use diuretics and maintenance fluid restriction (50mls/kg/day)
Ensure adequate haemoglobin
- Red cell transfusion may improve preload and oxygen delivery
- Ensure normal heart rhythm
- Cardioversion or cautious administration of anti arrhythmics may be required
- Vasoactive Agents: optimise afterload and contractility
- Vasopressors
- Inotropes
- Vasodilators (eg nitrates, but use carefully/avoid unless specialist support or advice)
- Resuscitation dose of Adrenaline
Prostaglandin (PGE1) therapy
- Used to maintain ductal patency in newborns and young infants with shock secondary to duct dependent congenital heart defects.
Infusion dose is 0.05-0.1mcg/kg/min.
Hypotension and apnea are important side effects.
- Normothermia
- Avoid hypothermia and fever
Placement of an arterial catheter for monitoring of blood pressure and blood
sampling, plus a central venous catheter for the infusion of fluids and vasoactive agents is desirable
furosemide infusion has less instability and can be switched off if worried that the BP is dropping rather than improving (and switch to fluid boluses instead)
Extracorporeal life support (ECLS) and ventricular assist devices (VADs) are the two forms of mechanical circulatory support currently available in certain centres to infants and children with cardiogenic shock not amenable to conventional therapy.
blood gas can help differentiate acute from chronic congestive heart failure (CHF). Metabolic acidosis and lactic academia
are usually present in patients with acute CHF with low cardiac output, while pH is usually normal and partial pressure of carbon dioxide (PaCO2) low in case of chronic CHF.
reduced vs preserved ejection fraction (inc causes - 4 for rEF, 6 for pEF); 2x ix, cardiomyopathies (dilated 12 causes, hypertrophic 3 causes, restrictive 5 causes)
1) Heart failure due to reduced ejection fraction (HFrEF):”systolic heart failure”. HFrEF is associated with an ejection fraction less than 40%.
2) Heart failure with preserved ejection fraction (HFpEF): “diastolic heart failure”HFpEF occurs when the left ventricle contracts normally during systole, but the ventricle is stiff and does not relax normally during diastole, which impairs filling
HFrEF: MI, dilated cardiomyopathy, myocarditis, valvular heart disease
HFpEF: LVH, hypertension, HOCM, restrictive cardiomyopathy, amyloid/sarcoidosis, valvular heart disease
echo and cardiac MRI can be helpful to investigate the cause
dilated: damaged myocardium (idiopathic, post-MI, late sequelae of myocarditis (esp coxsackie B), chagas, TB, pregnancy, alcohol use disorder, sarcoid/CTD, thiamine def, tachycardia, genetics)
hypertrophic: HOCM, friedrichs ataxia, fabry disease
restrictive: genetic, amyloid, sarcoid, HH, scleroderma, and more
cardiomyopathy (dilated inc 2 sx, who has highest incidence, 9 causes, 3 mx), hypertrophic main cause + 2 others, restrictive (15 causes), takotsubo ix and mx, peripartum definition, mx and prognosis; 3x chemo agents; tachycardiomyopathy pathophys, prognosis, when you get (3 things), pacemaker induced (definition, strong association and reason, mx)
dilated - causes heart failure, arrhythmias; children under 12mo have highest incidence, 1:2500 in adults; primary/idiopathic most often; other causes: myocarditis (esp enteroviruses like coxsackie, adenoviruses, parvovirus), toxins like alcohol, cocaine, doxorubicin; beri-beri, Chagas, hyper/hypothyroid, ischaemia and more; manage heart failure; ICD may be needed if Vtach, BV pacing if brady-arrhythmias
hypertrophic - HOCM is main one, friedrich ataxia + fabry others
restrictive - infiltrative (sarcoid, amyloid), storage (haemochromatosis, fabry, gaucher, niemann pick, mucopolysaccharidosis, glycogen storage disease), scleroderma, diabetic, myofibrillar or sarcomeric problems, hypereosiniphillic syndrome, carcinoid heart disease, metastasis, chemo/radiotherapy
takotsubo - stress induced, often presents with angina and can have ischaemic changes on ECG and trop rise but arteries clear on angio; apical hypokinesis; diuretics, ACEi, BB
peripartum - HF towards end of pregnancy or within 5 months of delivery, reduced ejection fraction, no other explanation; if haemodynamically stable can do vaginal delivery, if unstable then ECS; 20-70% recover, often within 6mo, but 10% die within 2 years; can breastfeed unless unstable
chemo - doxorubicin, tastuzumab, paclitaxel
tachycardiomyopathy - Atrial and/or ventricular dysfunction—secondary to rapid and/or asynchronous/irregular myocardial contraction, partially or completely reversed after treatment of the causative arrhythmia; subclinical ischaemia, Ca overload, redox damage; get spheroid dilation, thinning of wall, falling CO; normally much improved within 3mo of controlling the tachycardia (or frequent PVCs); generally get if PVCs >10-20% of beats, rate >100bpm or tachy >10-15% of day
pacemaker induced - will develop in 1 in 8 patients who receive a permanent pacemaker for complete heart block with normal ejection fraction; defined as a reduction in left ventricular ejection fraction (LVEF) of >10% after pacemaker placement; right ventricular pacing burden greater than 20 percent is most strongly associated with development of PICM, due to dyssynchronous ventricular contraction; upgrade to CRT is effective mx; must exclude other causes of reduced LVEF
clubbing grades and pathology theories
5 grades
No visible clubbing - Fluctuation (increased ballotability) and softening of the nail bed only. No visible changes of nails.
Mild clubbing - Loss of the normal <165° angle (Lovibond angle) between the nailbed and the fold (cuticula). Schamroth’s window is obliterated. Clubbing is not obvious at a glance.
Moderate clubbing - Increased convexity of the nail fold. Clubbing is apparent at a glance.
Gross clubbing - Thickening of the whole distal (end part of the) finger (resembling a drumstick)
Hypertrophic osteoarthropathy - DIP and MCP joints swollen and painful
clubbing causes: related to hypoxia? theories inc growth factor secretion from lungs, prostaglandin synthesis, vasodilation, megakaryocytes bypassing breakdown
in lung and getting trapped in fingers where they release PDGF and VEGF; right to left shunts allow newly-released megakaryocytes to escape the pulmonary circulation, and instead become lodged in nail bed capillaries where they release growth factors that cause increased capillary permeability and connective tissue hypertrop
clubbing causes (6:4:31:, 2 to think of first if in kids)
Lung disease:
Lung cancer, mainly non-small-cell (54% of all cases)
Interstitial lung disease most commonly idiopathic pulmonary fibrosis
Complicated tuberculosis
Suppurative lung disease: lung abscess, empyema, bronchiectasis, cystic fibrosis
Mesothelioma of the pleura
Sarcoidosis
Heart disease:
Any disease featuring chronic hypoxia
Congenital cyanotic heart disease (most common cardiac cause)
Subacute infective endocarditis
Atrial myxoma (benign tumor)
Tetralogy of Fallot
Gastrointestinal and hepatobiliary:
Malabsorption
Crohn’s disease and ulcerative colitis
Cirrhosis, especially in primary biliary cholangitis
Hepatopulmonary syndrome, a complication of cirrhosis
Others:
Graves’ disease (autoimmune hyperthyroidism) – in this case it is known as thyroid acropachy
of all of these, think congen heart disease and CF first if see in kids
lower limb oedema causes (8 of b/l + 5 drugs)
Heart failure
Constrictive pericarditis
Venous stasis
Lymphoedema
Nephrotic syndrome (+other causes of hypoalbuminemia)
Liver disease/cirrhosis
Hypothyroidism
Immobility
Drugs
most commonly used drugs which can cause oedema are:
* calcium channel blockers
* NSAIDs)
* corticosteroids
* hormones and related compounds e.g. tamoxifen, *mirtazapine
dyspnoea and position - CCF vs PE
Patients with acute heart failure and pulmonary oedema (accumulation of fluid in the alveoli) usually prefer to be upright, while patients with massive pulmonary embolism are often more comfortable lying flat and may faint (syncope) if made to sit upright
Orthopnoea, dyspnoea on lying flat, may occur in patients with heart failure - may be confused with asthma, which can also cause night-time dyspnoea, chest tightness, cough and wheeze, but patients with heart failure may also produce frothy white or blood-stained sputum.
aortic stenosis (inc 5 causes, 3 sx + pulse signs, other s/e, 1 ix, 2 meds for symptom relief, ind for surgical mx and what surg mx isinc two reasons to choose bioprosthetic, and what anticoag for biopros vs mechanical)
2% of people >65, male more common
acquired due to calcification and degen (ageing due to stress on the valve over time), rheumatic fever, pagets disease of bone, end stage renal failure, ochronosis; may be congenital due to bicuspid aortic valve (in 1-2% live births, causes more turbulence which leads to more calcification and fibrosis of leaflets)
risk factors are usuals IHD, hypertension, DM, lipids
compensatory LVH until LV failure
triad of angina, syncope, dyspnoea (angina from the LVH and subsequent inc wall pressure giving dec’d endocardial perfusion), syncope as cant inc CO on exertion; VWF may be sheared by the stenosis giving von willebrands disease; prognosis is 5yr with angina, 3yr with syncope, 2yr with dyspnoea
slow rising, small pulse volume, JVP, systolic thrill in aortic area (2nd ic space on right) during expiration; systolic ejection murmur radiating to carotid; echo + doppler to assess
no medical management: beta blockers may improve bloodflow, loop diuretics to relieve preload
Consider referring adults with asymptomatic severe aortic stenosis for surgery if
* Vmax (peak aortic jet velocity) more than 5 m/s on echocardiography
* aortic valve area less than 0.6 cm2 9 on echocardiography
* LVEF (left ventricular ejection fraction) less than 60% on echocardiography
* BNP/NT-proBNP level more than twice the upper limit of normal
* symptoms unmasked on exercise testing.
Consider referring adults with symptomatic low-flow low-gradient aortic stenosis with LVEF less than 50% for intervention if they have all of the following:
* mean gradient across the aortic valve less than 40 mmHg on echocardiography
* a valve area less than 1.0 cm2 19 , which does not increase on dobutamine stress echocardiography
aortic valve replacement is best shot - mechanical unless >65yo or cant be anticoagulated long term then bioprosthetic, as doesn’t need long term anticoag but wears out in 10-15 years where mechanical needs anticoag but doesnt wear out - also note warfarin should be used for this anticoag, DOACs not used
mitral regurgitation (damage to which 4 structures can cause, acute causes x3, chronic causes x5, 2 main problems in acute, what happens in chronicto prevent those problems; sx (3x for acute, 5 for chronic), 4 signs; ix, 2 modes of dying in chronic and what at inc’d risk of; 1 medical mx sometimes needed; 3 inds for surgery and 2 approaches inc when each preferred)
leaflets, chordae, pap muscles or LV damage can lead to MR
acute due to infective endocarditis, MI, trauma; chronic due to myxomatous (age related) degen, chronic rheumatic heart disease, heart dilatatation, hypertrophic cardiomyopathy, mitral valve prolapse
acutely LA pressure raised giving pulmonary oedema, and reduced ejection fraction giving low CO; in chronic LA enlarges and pressure normalises, LV dilates to maintain ejection fraction but ultimately this leads to failure
acute is a medical emergency: pul oedema, hypotension, cardiogenic shock
chronic asymptomatic to start then fatigue, exertional dyspnoea, orthopnoea, palpitations, AF
AF may give irregularly irregular pulse, systolic thrill at apex which is often displaced, large a wave in jvp; pansystolic murmur at apex radiating into axilla;
echo to evaluate
33% survival at 8 years w/o surgery, death usually due to heart failure but sometimes sudden death (arrhythmia related possibly)
at inc’d risk for endocarditis
anticoagulation if AF
surgery if
* LVEF less than 60% on echocardiography
* ESDI more than 2.2 cm/m2 5 on echocardiography
* an increase of systolic pulmonary artery pressure to more than 60 mgHg on exercise testing
valve repair preferred to replacement unless repair unlikely to work eg pap muscle rupture or extensive endocarditis damage
infective endocarditis (four things to make you suspect, five ways it affects heart, eleven immune complex phenomena, three signs of longstanding infection, 3 major and five major duke criteria)
highly variable, may be insidious
unexplained fever, cardiac lesion, bacteraemia, embolic phenomena (from clotting in endocardium shedding emboli) should give high index of suspicion but hard to diagnose
valve destruction may give a murmur, progressive heart failure giving oedema; AV block in 2-4% patients as infection extends into septum, may get abscess or pericarditis
immune complex deposition giving: petechiae, splinter haemorrhages, oslers nodes, janeway lesions, roth spots, conjunctival splinter haemorrhages, retinal flame haemorrhages, microscopic haematuria, glomerulonephritis, arthralgia/arthritis, toxic encephalopathy
longstanding infection: hepatomegaly, clubbing, anaemia
major criteria: positive blood culture, echo showing oscillating intracardiac mass (vegetation), abscess, new valve regurg or dehiscence of prosthetic
minor: fever >38, IVDU (always consider in any patient who has lots of venous access), vascular or immunological phenomena
investigating and managing inf endo
3-4 blood cultures from separate sites an hour apart
FBC, LFTs, U&Es, urinalysis, echo (+/- pet CT)
be guided by microbiology for antibiotics to use
IE first time is amox + gent, vanc and gent if sepsis or embolic features, add rifampicin if prosthetic valve
change once you have culture results
generally iv for 2 weeks and total for 4-6, then stop if patient well and follow in outpatient
colon cancer can lead to endocarditis by allowing bacteria to get from gut into blood then to heart; strep bovis and strep gallolyticus are two such bugs that may be caused by this
staph aureus causes acute or subacute endocarditis; GAS and GBS can also cause acute; most other strep (inc viridans) + HACEK and fungi cause subacute; aureus tends to be more destructive
HACEK endocarditis - what it is, what endo is normally due to, stands for what, affects what kind of pts and how long diagnosis usually delayed, why the delay, hence consider when
all HACEK members are fastidious Gram-negative bacteria associated with infective endocarditis
Most endocarditis is caused by Gram-positive bacteria (most commonly Staphylococcus or Streptococcus) with a minority caused by Gram-negatives or fungi; all live in the oropharynx as commensals
acronym stands for Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella
HACEK endocarditis mostly affects most patients with heart disease or artificial valves, and is characterized by an insidious course, with a mean diagnosis delay of 1 month
Various studies have shown that these microorganisms have low growth or no growth in blood culture and this may lead to delay in diagnosis -> consider if negative cultures; note however most other organisms may also be culture negative
libman sacks endocarditis (aka, what it is, commonest on which valve, seen commonly in what 3 conditions and 3 other linked conditions; general sx, 3ix, medical mx x2 and surgical indications x3)
aka marantic endocarditis; sterile vegetations on the valves
most often on mitral valve but can be on any
initial development of Libman-Sacks endocarditis appears to be an endothelial injury in the setting of a hypercoagulable state. So they are mainly observed in patients with malignancies (mainly solid tumor: adenocarcinoma - 2.7% of these pts), systemic lupus erythematosus (SLE - 6-11% but autopsies suggest as many as 50%) and antiphospholipid syndrome (33%); also has been reported in pts with DIC, sepsis, rheumatoid arth; note also that ppl with SLE may dev antiphospholipid syndrome
oft asymp, but can have embolic phenomena esp TIA, stroke, mesenteric or limb ischaemia, as well as more minor embolic phenomena too; it is also rare for valve dysfunction to occur
if suspect then TTE, TOE if inconclusive; work up for hypercoag risk factors, and treat cause + consider anticoag; surgery as with IE if heart failure or acute valve dysfunction, can also be done if multiple embolic events
postural hypotension (neurogenic causes x4, non-neurogenic x8, medication x7, 6 sx, main ix inc how to do, positive result x3, mx x2)
postural hypotension: neurogenic (DM, parkinsons, (small cell) lung carcinoma, monoclonal gammopathy)
non-neurogenic inc arrhythmias, aortic stenosis, HOCM, otherwise reduced CO, dehydration, adrenal insuff, vasodilation (inc fever), anemia
medications (diuretics esp thiazides, alpha blockers (end in osin), antihypertensives, insulin, levodopa, TCAs, cannabis
dizziness, weakness, confusion, nausea, blurred vision (all on standing), syncope
must do lying/standing blood pressure in elder w fall and anyone else with these sx
Ask the patient to lie down for at least five
minutes.
Measure the BP.
Ask the patient to stand up (assist if needed).
Measure BP after standing in the first minute.
Measure BP again after patient has been standing for three minutes.
Repeat recording if BP is still dropping.
In the instance of positive results, repeat regularly until resolved.
Notice and document symptoms of dizziness, light-headedness, vagueness, pallor, visual disturbance, feelings of weakness and palpitations
A positive result is:
A drop in systolic BP of 20mmHg or more (with or without symptoms).
A drop to below 90mmHg on standing even if the drop is less than 20mmHg (with or without
symptoms).
A drop in diastolic BP of 10mmHg with symptoms (although clinically less significant than a
drop in systolic BP).
mx of postural hypotension is midodrine or fludrocortisone, max out on one then the other
hypotension - parkinsons drugs that cause, drugs used to treat (inc main s/e for one)
PD drugs: dopamine agonists (pramipexxole, ropinirole), sometimes l-DOPA
to treat midodrine and fludrocortisone
midodrine is prodrug for alpa1 agonist, can cause urinary retention
fludrocort is MR agonist
evaluation of orthostatic hypotension - what normally happens when stand (inc how much pools), normal changes x3, causes (7 CV, 2 volume, 6 endo, 9 drugs, 3 misc, 7 neuro), 7ix, 5 mx
Standing results in blood pooling of approximately 500 to 1,000 mL in the lower extremities and splanchnic circulation. This initiates an increase in sympathetic outflow
These compensatory mechanisms result in a decrease in systolic blood pressure (5 to 10 mm Hg), an increase in diastolic blood pressure (5 to 10 mm Hg), and an increase in pulse rate (10 to 25 beats per minute)
CV: anemia, heart failures, valves (AS), arrhythmia, MI, myo/pericarditis, caval compression
volume: bleed, dehydration
endo: adrenal insuff. polyuria, hyperglyc, hypokal, hypothyroid, phaeochromocytoma
drugs: diuretics, sedatives, antiHTNs, antiPD, anticholinergics, antiadrenergics, antanginals, antidepressants, antiarrhythmics
misc: eating disorders, anxiety, prolonged bed rest
neurogenic: PD, amyloidosis, autonomic failure, diabetic or B12 neuropathy, MSA, LBD
ix: FBC, U&Es, TFTs, 9am cortisol, B12 levels, ECG, echo
mx: assess fluid responsiveness and ensure well hydrated; treat cause if identified from above, including changing or reducing medications; if suspect chronic hyponatremia do 24-hr urine sodium collection and if low start Na supplementation; then fludrocortisone and midodrine
heart murmurs - 6 grades; AR 4 signs, 2 mx inc 3 surg inds, 2x monitoring options, two possibly needed mx if acute/severe, aortic root dilatation 8 risk factors and how causes AR, 3 other chronic causes of AR, 3 acute causes)
grades
One
Very faint. Heard by an expert in optimum conditions
Two
Heard by a non-expert in optimum conditions
Three
Easily audible, no thrill
Four
A loud murmur, with a thrill
Five
Very loud, often heard over a wide area, with thrill
Six
Extremely loud, heard without a stethoscope
(AR causes wide pulse pressure, collapsing pulse, nailbed pulsations, head bobbing with pulse; surgery if symptomatic, LVEF reduced <55%, ESDI (end-systolic diameter index) more than 2.4 cm/m2 on echocardiography
ACEi + monitor w echo annually (if dilated root) or biannually; in acute severe situations inotropes and vasodilators eg dobutamine and nitroprusside
aortic root dilatation, linked to age and also EDS/marfans/kawasakis/takayasus/behcets as well as HTN, smoking etc causes AR by stretching valve so it cant close properly, this is really a form of AAA and can dissect like others and is commonest cause of AR, can also be due to SLE, bicuspid valve, CTD w/o dilation of root; acutely consider inf endo, aortic dissection, trauma)
heart murmurs - 9 types (phase, additional descriptor, louder on insp or exp, location, radiation (if any)
Aortic stenosis Systolic Ejection systolic Expiration 2nd intercostal space right sternal edge Carotid arteries
Pulmonary stenosis Systolic Ejection systolic Inspiration 2nd intercostal space left sternal edge Left shoulder/infra-clavicular
Mitral regurgitation Systolic Pansystolic Expiration Apex Axilla
Tricuspid regurgitation Systolic Pansystolic Inspiration Left sternal edge
Mitral valve prolapse Mid systolic + opening click Expiration Apex
Aortic regurgitation Early diastolic Decrescendo Expiration Left sternal edge (or 2nd intercostal space right sternal edge) Left sternal edge
Pulmonary regurgitation Early diastolic Decrescendo Inspiration 2nd intercostal space left sternal edge
Mitral stenosis Mid/late diastolic Expiration Apex
Tricuspid stenosis Mid/late diastolic Inspiration Left sternal edge
murmur quadrants in kids (inc where septal defect murmurs heard)
line through midsternum, line through level of nipples; which quadrant is it loudest in?
if below nipples is pansys, above is ejectionsys
ruq: aortic stenosis, rlq: tricuspid regurg, llq: vsd, mitral regurg, stills murmur, luq: pulm flow murmur, pulm stenosis, asd, pda (ejection sys in younger infants, continuous machinery murmur in older children)
functional murmurs (6 general features, 3 main kinds)
asymp systolic, short, <3/6 grade, normal S2, change with posture
venous hum: blood coursing through large veins in neck, gives blowing continuous murmur just below clavicles and varies with neck position and resp
pulm flow murmur: soft ejection sys murmur
vibratory/stills murmur: short buzzing murmur over left lower sternal edge/apex which changes with posture and usually disappears by puberty
the three innocent murmurs and how to mx them x3 and 4:3 features
stills murmur heard best lying down, over left sternal border; venous hum heard best sitting/standing up; pulm flow murmur benign in pulm area
if sure it is innocent then no further ix/mx needed
if unsure and <1yo refer routinely to cardiology clinic
if unsure and >1yo get ST4+ to review, if innocent or sure mx as above and if features not consistent with innocent then routine referral to cardiology clinic
features: <4/6, no radiation, not diastolic, normal peripheral exam; usually also: short, change with position, musical or vibratory
syncope/presyncope (10 inc 15 drugs)
Arrhythmias Postural hypotension Aortic stenosis Hypertrophic cardiomyopathy POTS Atrial myxoma
Vasovagal
epilepsy
anxiety
drugs (methyldopa, antiarrhytmics, prazosin/doxazosin, beta blockers, diuretics, nitrates, ACEi, CaV, hydralazine, sildenafil, oxybutynin/anticholinergics, levodopa, MAOI, TCAs, baclofen)
9 abnormal first heart sounds causes
quiet: Low cardiac output * Poor left ventricular function * Rheumatic mitral regurgitation * Long P–R interval (first-degree heart block)
loud: Increased cardiac output * Large stroke volume * Mitral stenosis * Short P–R interval * Atrial myxoma (rare)
s2 abnormalities (phys splitting, wide/reverse splitting x 4, quiet and loud)
Physiological splitting of S2 occurs because left ventricular contraction slightly precedes that of the right ventricle so that the aortic valve closes before the pulmonary valve. This splitting increases at end-inspiration because increased venous filling of the right ventricle further delays pulmonary valve closure. The separation disappears on expiration
may be quiet in aortic stenosis, loud in systemic or pulmonary HTN
wide splitting if delay in RV emptying eg RBBB or pulmonary HTN, or ASD as this leads to RV volume being larger than left
reversed splitting if LV emptying delayed in eg LBBB or left vent outflow obstruction
additional heart sounds (4 - 4:1:1:1)
3rd normal if febrile, pregnant, <30yo - otherwise think LVF, MR (in heart failure may see S3 with tachycardia aka gallop rhythm)
4th just before S1 and caused by stiff ventricle eg LVH
opening snap in mitral stenosis after S2, ejection click after S1 in aortic stenosis
TLOC (syncope most common cause, 2 things suggesting cardiac origin, 3rd common syncope cause; and differing VV from seizure - 7 things to consider)
Syncope is loss of consciousness due to inadequate cerebral perfusion and is the most common cause of transient loss of consciousness (TLOC). Vasovagal (or reflex) syncope (fainting) is the most common type and precipitated by stimulation of the parasympathetic nervous system, as with pain or intercurrent illness. Exercise-related syncope, or syncope with no warning or trigger, suggests a possible cardiac cause. TLOC on standing is suggestive of orthostatic (postural) hypotension and may be caused by drugs (antihypertensives or levodopa) or associated with autonomic neuropathies, which may complicate conditions such as diabetes
to tell vasovagal from seizure - was there a prodrome? a trigger? <60s or 1-2min duration, convulsions (and if so brief myoclonic jerks in vasovagal and tonic clonic in seizure), colour, any injuries (myalgia, lateral tongue biting, headache, back pain, dislocations all more likely with seizure), and how fast is recovery inc postictal phase
the second heart sound (reason for split, 3 causes of wide split, 3 causes of reversed split, 2 causes of narrow split, 4 causes of single S2)
v important in paeds
normally aortic valve closes before pulm as higher closing pressure in sys circulation so normal S2 has physiological splitting and increases on inspiration
wide splitting caused by RBBB or pulmonary stenosis, fixed wide splitting by ASD
reversed splitting (pulm component before aortic)due to LBBB, severe aortic stenosis, LV failure
narrow splitting due to pulm HTN or aortic stenosis
sys hypertension causes loud aortic component and pulm HTN loud pulm component
single second heart sound due to tof, pulm atresia, single ventricle, aortic atresia
rheumatic fever (5 major and 6 minor Jones criteria, 6 dd, 4 mx)
may or may not have history of fever, then 2-4 weeks later:
migratory polyarth, carditis (some combo of myo, endo, or peri - look for new murmurs, tachycardia greater than fever), sudenhams chorea (several weeks-months after initial infection, usually not if cardiac involvement, child will be fidgety with sudden involunary movements and maybe altered speech), erythema marginatum (non-pruritic maculopap rash on trunk and limbs with central clearing), subcut nodules (extensor surface, also scalp or spine)
minor inc fever, arthralgia, prev rheum fever (ie can recur), raised acute phase proteins, leucocytosis, prolonged PR (and if pericarditis ST segments may be raised, if myocard T waves may be flattened or inverted)
2 major or one maj 2 minor + evidence of prev step infection (increased antistreptolysin antibodies titre, pos throat culture, recent scarlet fever)
also consider: SLE, juvenile chronic arth, lyme disease, leukaemia, gonococcal disease, kawasaki disease)
treat: rest, high dose aspirin, steroids if carditis, prophylaxis against recurrence with oral or im penicillin
cardiomyocytes and ventricle AP
up to 10 microns in diameter and not more than 200 in length, mechanically and electrically coupled together by intercalated discs to form a syncytium:desmosomes linke mechanically and gap junctions electrically; SR less developed than in skeletal and dyads rather than triads; some cells specialised for impulse generation/conduction
AP remains depolarised for prolonged period, especially in ventricles, remaining at ~0mV for as long as 500ms and arising from prolonged inwards Ca current, amplitude varying with[Ca]ext and diminished by Ca channel blockers like verapamil/nifedipine; 5 phase ventricle AP: phase 0 = rapid depolarisation, phase 1 = initial repolarisation phase 2 = plateau phase 3 = terminal repolarisation and stage 4= electrical diastole; during plateau membrane R increased due to activation of inward rectifying K channels which minimises Ca gradient dissipation by reducing required inwards current; more K channels open to repolarise
pacemaker cells and spread of electrical activity in heart
net inward ionic current generates gradual depolarisation to threshold; group of cells with fastest rate set the HR, normally SA (60-80 discharges per min); AVN (40-50) purkinje fibres (30-40) can take over in eg sick sinus syndrome and contraction cells can’t usually generate a pacemaker current; SAN will depolarise without extrinsic innervation
intercalated discs have low electrical impedance allowing current to propagate between cells; AVN conducts slower than myocardium (0.2m per s) to synchronise atrial/ventricular contraction; bundle of His/purkinje fibres have less myofibrils and conduct faster than surrounding myocytes (2-5m/s vs 1m/s); absolutely refractory in first part of AP until repolarisation to ~-40/-50mV due mainly to Na channel inactivation, relatively refractory until complete repolarisation, meaning evoked AP has smaller amplitude and slower rate of rise; refractory period duration thus relates to AP duration (ie ventricle longer than atrial, shorter than purkinje), this serves to ensure propagation just once to prevent re-entry arrhythmia; impossible to induce tetanic contraction in heart
EC coupling in heart - how Ca release differs in cardiac muscle from skeletal
troponin has 3 rather than 4 binding sites; increase in cytosolic Ca and tension closely track AP timecourse; SR most important source, but also enters during plateau phase; doubling IF Ca may double max tension, unlike in skeletal as this Ca is stimulus for more Ca release (l-type VG Ca open, Ca enters and opens Ryr on SR); skeletal releases quantity of Ca well in excess of that needed for max tension, in heart Ca release isn’t supramaximal but linked to factors which influence inotropy; skeletal muscles modulates contraction strength by recruiting more fibres but cardiomyocytes linked so modulate based on how much Ca made available to myofilaments; Ca influx replenishes intracellular stores so after imposed period of quiescence first contraction is markedly reduced; Ca pumps in SR and PM, Na/Ca exchange in PM using Na gradient from Na pump (digoxin etc)
cardiomyocyte force/length relationship and autonomic effects on heart conduction
passive length-tension curve considerably steeper than for skeletal, so much more resistant to stretching; consequently almost all active shortening on part of curve where increased stretch gives increased contractile force; starling mechanism, bowditch (ensure adequate SV when time for contraction reduced) and anrep effects
Vagus via ACh slows HR (negative chronotropic) by increasing PM K conductance (by activating muscarinic GPCRs which opens K channels) to hyperpolarise the membrane of SAN during diastole; may also reduce force of contraction by reducing inwards Ca current; NA/adrenaline affect HCN and Ca current to increase rate of pacemaker depolarisation (positive chronotropic) and increase inward Ca current (positve inotropic) giving plateau with higher but shorter peak
ecg basics (u waves, sq to ms conversion, PR/QRS/QT lengths and what happens in each bit), how big should calibration point be (and what else to check), what each lead looks at, axis deviation, what is normal cardiac axis and which lead is at each end of this, what if S >/=R, normal shape of V1-6 inc where is septum
u waves may follow t waves and look like a second bump; may represent repol of pap muscles; is normal if after normal shaped T wave, may be pathological if the t wave flattened
large 5mm sq represents 200ms so 5 large squares per sec, 300 per min; an ECG strip is 10s long
PR interval is actually from start of p to start of qrs and is time for initiation, atrial contraction, propagation via bundle of His; normally 120-220ms aka 3-5 small sq; QRS is time for ventricle depol and usually 120ms aka 3 small sq or less; note this is just depol time not vent contraction which occurs during ST segment; if QT is prolonged >450ms may lead to vent tachy
the calibration point should be two large squares (and check rate ecg was run at)
I, II, VL look at left lat heart, III and VF at inf surface, VR at right atrium; note this is vertical plane
V1-6 look in horizontal plane; V1 and 2 look at right ventricle, V3/4 at septum and ant wall of left vent, V5/6 at ant/lat walls of left vent
so to tell axis: leads VR and II look at heart from opp directions so II should be pos and VR neg; normal depol is 11 oclock to 5 oclock and hence leads I, II, III should be pos with biggest deflection in lead II; right vent hypertrophy causes axis to swing to right so lead I becomes neg and lead III more pos, this is right axis deviation; left axis deviation is the opposite and becomes significant when lead II is also negative; as well as hypertrophy, left axis deviation can represent conduction defect
normal cardiac axis is -30deg (where VL sits) through to +90 deg (where VF sits)
if S wave>R wave then conduction is >90deg from a lead, if S=R then conduction is at 90deg so if S=R in lead I then axis is at 90deg so S>R in this lead then right axis deviation
for V1-6 QRS complex: right vent is first pos deflection, left vent first neg deflection, then neg deflection in right vent (outweighed by bulk of left vent) and pos deflection in left vent; V1 is thus mostly neg and V6 mostly pos, point where R and S waves equal shows position of septum; note also extremes that V1 is just small R big S and V6 small Q large R; enlarged rv moves transition point from V3/4 to V4/5 or V5/6 and this rotation is classic ecg sign of chronic lung disease
long PR definition/causes (10), wide QRS meaning and 2 broad causes inc how to differentiate, for first cause which type common which always pathological, appearance; how fascicle blocks appear
PR prolonged over 5 small squares/200ms suggests first deg heart block, itself a sign of eg fibrosis of the AV node, high vagal tone, medications that slow the AV node such as beta-blockers (digoxin, adenosine, Cav blockers, amiodarone), hypo/hyperkalemia, hypothyroidism, acute rheumatic fever, MI, sarcoid/HH/amyloid, or carditis associated with Lyme disease or SLE
wide QRS means ventricles contracting separately (as width corresponds to time ventricles spend depolarising between them) suggests bundle branch block or depol initiating in vent muscles due to complete heart block, but if P waves present with normal PR interval and wide QRS then bundle branch block
RBBB quite common in normal people but can be pathological, LBBB always pathological (STEMI); in RBBB, due to inc’d time for rv to depol there is second R wave in V1 and and wide/deep S wave so V1 mostly neg, wide QRS in V6; in LBBB small Q in V1 followed by R so V1 mostly pos, and in V6 R wave followed by small S (oft only appearing as a notch); then as LV depols get S wave in V1 and another R in V6; LBBB often has inverted T waves in some or all of the lat leads (I, VL, V5/6); so look for RSR (M) mostly neg in V1 for RBBB, and look for broad QRS with notched top in V6 for LBBB and this looks like an M (may see in other lat leads too), may be a W shape in V1 too (mostly pos) but this oft poorly developed
left bundle has ant and post divisions, if left ant fascicular block then appears as left axis deviation; rare for left post fascicle to be blocked but would get right axis deviation if so; RBBB with left axis deviation suggests right bundle and left ant fascicle blocked and so extensive damage to conduction system
heart rhythm on ecg (sinus brady and tachy causes and sinus arrhytmia definition, whihc rhythms are supravent and how these relate to qrs andwide qrs, bradycardia and electrical pathways, extrasystoles - cause, appearance + telling from escape beats; carotid sinus pressure mechanism, atrial fib appearance, what kind of tachy do junctional tend to be?)
sinus bradycardia from being highly trained athlete, hypothermia, myxoedema, oft seen immediately after heart attack too; sinus tachy suggests exercise, fear, pain, haemorrhage, thyrotoxicosis; a sinus arrhytmia has one P per qrs, constant PR interval, beat to beat change in R-R interval
may also initiate in atrial muscle, AVN (junctional), or vent muscle; sinus, atrial, and AVN are collectively supraventricular rhythms; spread via bundle of His and thus QRS is normal but narrow; if vent initiation spread abnormally giving wide and abnormal QRS and strange T; so supravent: narrow qrs, vent: wide qrs; only exception is supravent with a bundle branch block, or in WPW syndrome - in both cases qrs will be wide
bradycardia may be due to escape pathway taking over when SAN fails due to slower intrinsic depol rates; suggests problem higher up in conducting pathway eg heart attack, with the (sinus in this case) bradycardia protective; intrinsic rates: AVN 40-60, bundle of His can be 30 or less
extrasystoles result from any part of conduction system depol before it should; look like an escape beat but whereas those are later than the p wave that failed to come, these are sooner; atrial extrasystole will have abnormal p wave, junctional no p wave, both with qrs matching sinus rhythm; vent extrasystole will have wide qrs of strange shape and common and usually harmless, unless overlap previous t wave as can then lead to vfib; supravent extrasystole resets p wave cycle, vent doesnt so next p wave is when it should be
carotid sinus pressure leads to vagal reflex with SA rate dec and AVN delay inc, thus supravent tachy may be abolished or else inc block between atria and ventricles making eg atrial flutter more obvious; no effect on vent tachy
no p waves, irregular baseline with irregularly timed but normal looking qrs suggests atrial fib
junctional tachy are usually re-entry tachy
abnorms of shape on ecg - 3 causes of wide qrs, RVH (inc PE characteristic pattern), LVH, q waves, st elevation and depression causes inc how NSTEMI will look, causes of t wave inversion (and where its normal for them to be neg), electrolyte effects, extrasystoles and risk of heart problems, how to reduce PVCs, STEMI criteria
wide qrs due to bundle branch blocks or vent focuses, or wpw
height inc suggests inc muscle mass; RV hypertrophy will have V1 become pos as R becomes larger in mag than S, and deep S wave in V6, may also see right axis deviation and sometimes T wave inversion in V1/2m sometimes even V3/4; so a PE may show: right axis deviation, prominent peaked p waves (ra hypertrophy), tall R waves in V1, RBBB, inverted T waves in V1/2, maybe V3/4, shift of transition point to V5/6; ecg changes may not occur with PE; also S1Q3T3
left vent hypertrophy causes tall R in V5/6 and deep s in V1/2, T wave inversion in lat leads, sometimes left axis deviation
Q waves >1 small sq in width and 2mm deep indicate MI as death of muscle creates cavity with all depol moving away from it; Q waves in V2/3/4/5 suggest ant MI, ant lat in V3/4 and I, VL, V5/6; inf MI in III and VF; these will be present in old infarctions too, anywhere with dead muscle; elevated ST suggests recent infarction or pericarditis and again affected leads suggests location; pericarditis will cause ST elevation in most leads as not localised; ST depression usually suggests ischaemia not infarction, as in exercise, esp in angina; if ST segment depressed but downward sloping rather than horizontal suggest digoxin
NSTEMIs dont have full thickness infarction so no ST elevation and no q waves; T wave inversion usually occurs when (if) q waves appear
inverted T waves also in hypertrophy and bundle branch block; T waves should be neg in VR and V1, sometimes III and V2, sometimes V3
note pathological q waves may replace a previous RS or QRS
hypokalaemia flattens T waves and causes U waves to appear; hyperkalaemia causes peaked T waves, ST segment to disappear, sometimes QRS to widen; hypocalcaemia prolongs QT interval and hypercalcaemia shortens it
supraventricular extrasystoles have no clinical significance; frequent vent extrasystoles suggests risk of dev’g heart problems at pop but not indi level, but occasional ones are completely normal; reducing alcohol and caffeine intake can reduce these
STEMI needs 1mm elevation in 2+ contiguous limb leads, or 2mm elevation in 2+ contiguous chest leads; or a new onset LBBB
posterior STEMI
ST depression V1-V4, R/S ratio >1 V1/2, ST elevation in V7/8/9 if applied; may be coexistant inferior STEMI
usually from occlusion of lCX but can be right coronary; usually also get inferior or lateral infarction too
coronary artery origins, what determines dominance, 2-3 branches of LMS, LAD branches and segments and localising lesion in LAD, branches of the RCA and the LCx
The aortic valve has three cusps, two of which give rise to the coronary arteries. The left coronary cusp gives rise to the left coronary artery. The right coronary cusp gives rise to the right coronary artery. The posterior non-coronary cusp does not usually give rise to a coronary artery.
Dominance of the coronary circulation is determined by which coronary gives rise to the Posterior Descending, a vessel supplying the apex of the heart. In 85% of cases, the PD is a branch of the right coronary artery, making it a right-dominant system. In 7% of cases, the PD is a branch of the LAD, making it a left-dominant system. In 8% of cases, the coronary circulation is co-dominant.
The Left Main coronary artery typically bifurcates into two branches, the left anterior descending artery (LAD) and the circumflex artery (Cx). Occasionally, a third branch called Ramus Intermedius may arise between the LAD and the Cx.
The LAD lies over the anterior aspect of the heart, courses through the anterior interventricular sulcus, a groove between the right and left ventricles. The LAD gives off several diagonal branches. These run diagonally on the anterolateral portion of the left ventricle. The first diagonal branch is designated as D1; the second diagonal branch is designated as D2; and so on. The first diagonal branch is used as an anatomic landmark in designating the different segments of the LAD. The segment of the LAD proximal to D1 between the origin of the LAD and the origin of D1 is called the proximal LAD. The most distal 1/3 of the LAD is
called the distal LAD. The segment of the LAD between the proximal LAD and distal LAD is the mid-LAD. The LAD also gives off several branches called septal perforators (SP), which supply blood to the interventricular septum.
proximal LAD occlusion affects V1-4, aVL, lead I; septum (V1) often spared if occlusion after septal branch but before 1st diagonal; if also distal to 1st diagonal will spare septum and basal wall, so no affect on V1, aVL, lead 1
The right coronary artery (RCA) runs through the right atrioventricular sulcus, a groove between the right atrium and right ventricle. The RCA gives off several branches including the SA-nodal artery in most people, the acute marginal (AM) branch, the AV Nodal artery and usually the posterior descending artery
the circumflex gives off obtuse marginal (OM) branches
note again you can localise ST elevations, you can’t localise depression or even TWI
OMI
Occlusion Myocardial Infarction (OMI) - ECG patterns that don’t fit STEMI criteria yet nevertheless suggest acute coronary occlusion that would benefit from immediate percutaneous coronary intervention
Elevation of any degree in two contiguous inferior leads with any amount of ST depression in aVL is highly suspicious for inferior OMI
New RBBB and LAFB is highly associated with proximal LAD occlusion and negative outcomes. Raise suspicion for OMI, and look for subtle ST changes which may be more difficult to discern.
T waves out of proportion of preceding R waves, especially in the context of STE and/or reciprocal changes, should raise suspicion of OMI and impending classic STE changes
ST depression maximal in leads V1-4, without progression to V5-6, should be considered a posterior OMI until proven otherwise, even in the absence of ST elevation in leads V7-9
Multi-lead ST depression with coexistent ST elevation in lead aVR has been described in patients with left main or proximal LAD insufficiency causing severe ischaemia - urgent but not emergency PCI
SCAD (what it is, presents in who, 4 associations)
Spontaneous coronary artery dissection (SCAD) is a rare cause of myocardial infarction (MI), presenting mostly in healthy, young women
not associated with atherosclerosis or trauma
linked to the hormone changes of pregnancy, also FMD and eg EDS and marfans
T wave changes (normal size and direction, 6 abnorms and the causes of them)
normal: Upright in all leads except aVR and V1, sometimes lead III
Amplitude < 5mm in limb leads, < 10mm in precordial leads
peaked: Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia
hyperacute: Broad, asymmetrically peaked, early stages of a STEMI
TWI: normal in young children as right side dominant, also in bundle branch block, hypertrophy, HTN/strain/PE, hocm, ischaemia and infarction
- Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children, representing the dominance of right ventricular forces
- T-wave inversions in the right precordial leads may persist into adulthood and are most commonly seen in young Afro-Caribbean women. Persistent juvenile T-waves are asymmetric, shallow (<3mm) and usually limited to leads V1-3
- ischaemia: Dynamic T-wave inversions are seen with acute myocardial ischaemia
Fixed T-wave inversions are seen following infarction, usually in association with pathological Q waves
- Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6; Right bundle branch block produces T-wave inversion in the right precordial leads V1-3
- Left ventricular hypertrophy (LVH) produces T-wave inversion in the lateral leads I, aVL, V5-6 (left ventricular ‘strain’ pattern - so eg sys HTN)
-Right ventricular hypertrophy produces T-wave inversion in the right precordial leads V1-3 (right ventricular ‘strain’ pattern) and also the inferior leads (II, III, aVF) (so in eg pulm HTN)
-HOCM as deep TWI in all prechordial leads
-sudden rise in ICP (eg SAH/bleed) produce widespread deep T-wave inversions with a bizarre morphology
biphasic T waves: two main causes of biphasic T waves:
Myocardial ischaemia (up then down)
Hypokalaemia (down then up)
The two waves go in opposite directions
Wellen’s syndrome: pattern of inverted or biphasic T waves in V2-3 (in patients presenting with/following ischaemic sounding chest pain) that is highly specific for critical stenosis of the left anterior descending artery - so one of few ischaemic patterns you can localise.
There are two patterns of T-wave abnormality in Wellens syndrome:
Type A = Biphasic T waves with the initial deflection positive and the terminal deflection negative (25% of cases)
Type B = T-waves are deeply and symmetrically inverted (75% of cases)
Note: The T waves evolve over time from a Type A to a Type B pattern
camel hump: two peaks, either hypokal (U wave) or P wave part buried in T wave
flattened: ischaemia, hypokal
ionic mechanism of ST elevation, T wave changes
inciting event leading to ST elevations on an ECG is the inability of mitochondria within ischemic myocardial cells to generate enough ATP
one of the efflux K channels is Katp channel, and opens when ATP not present; therefore during ischemia more potassium is exported from the myocyte.
More potassium export in ischemic cells leads to faster ventricular depolarization of those cells relative to non-ischemic, well-perfused myocytes. The electrical cycle in ischemic cells becomes shorter, which in effect creates an electrical charge difference between ischemic and non-ischemic areas of the heart during depolarization.
As a result of the difference in charges there is a relative current (i.e., flow of charge). In this case the current flows from ischemic to non-ischemic myocardium.
In the leads that are over the ischemic myocardium, this is “away” from those leads since the ischemic area involves all of the myocardium under the lead up to the epicardium (remember, in a STEMI the ischemia is transmural).
This shifts the ECG in a negative direction (i.e., it is depressed on the tracing).
Because there is essentially no difference in repolarization speeds in ischemic and non-ischemic myocytes, once the ECG arrives at this section the gradient disappears and the EKG shifts back upward.
What we are left with is the following explanation for ischemic ST elevations: the ST segment only appears elevated because the baseline of the other ECG segments has been shifted down (as by convention the QT region is at the neutral 0 point)
With subendocardial ischemia (e.g., with an NSTEMI), the mechanism works exactly the same way; there is some non-ischemic tissue between ischemic myocardium and the ECG electrodes. This results in the opposite result finding on ECG. The ischemic current flows toward the electrode, shifting the ECG baseline up and the ST segments appear depressed
paediatric ecgs general approach (scale and amplitude, axis at birth, 1yo, 10yo, interpreting p waves, PR interval and 2 causes of neonatal complete heart block (and
3 signs of it), 2x q waves causes, amplitude for LVH and RVH, how dominance changes over time, 7 causes of long QT, how T waves change over time in V1 and V6)
remember 1mm is 0.04s and 10mm amplitude is 1mV
axis at birth is +60 to +180, then at 1yo +10 to +100, and at 10yo -30 to +90
p waves should precede a qrs, be positive in I, II, and aVF, should be <2.5mm
p waves >2.5mm suggest RA hypertrophy, bifid p wave lasting >0.09s is LA hypertrophy
PR interval reduced in WPW, enlarged in heart block; it should be 0.2s; neonatal complete heart block associated with maternal SLE due to anti-Ro ig or post cardiac surgery; will see spontaneous ventricular escape rhythm, variable first heart sound, giant A cannon waves in JVP due to atrial contraction against closed AV valves (also in vent/nodal tachy)
q waves >4mm deep and seen in ischaemia or hocm; RVH if R wave in V1>15mm, or over 10mm if over 3mo old; also see right axis deviation; LVH if R wave in V6 >20mm; right ventricular dominance (big R in V1 and big S in V6) as a newborn shifts to left ventricular dominance (big s in V1 and R in V6) by 3, showing normal QRS progression by this time; deviation in expected dominance also suggests ventricle hypertrophy
prolonged QRS in bundle branch block; QT interval should be 0.35-0.45s, increased in various congenital conditions or in hypocalc, hypomag, hypotherm, hypothyroid, rheumatic carditis, drugs
T waves invert in V1 by end of first week of life and revert by puberty; should always be upright in V6 and if inverted consider myocarditis or cardiomyopathy
ecg appearance of dextrocardia, WPW, atrial flutter/fib, RVH/LVH - and paediatric causes for latter 2 (5:6)
dextro - inverted p wave in lead I, upright in aVF, loss of normal qrs progression
WPW - shortened pr, delta wave, predisposes to paroxysmal SVT
atrial flutter has saw toothing with rate of 300, usually 2:1 block so ventricular response of 150/min but other block patterns possible - compare number of saws to QRSs; this and Afib commonest post-srugery, with CHD eg ebstein anomaly, other diseases resulting in dilated atria, and myocarditis
RVH from l->r shunts like VSD, ASD, PDA, right vent outflow obstruction from pulm atresia/stenosis, and cor pulmonale; LVH from left outflow tract obstruction (aortic stenosis or coarctation, ostium primum ASD, VSD, PDA, tricuspid atresia
WPW syndrome - pathphys, 3 main ECG findings, 5 arrhythmias, mx (acute, maintenance)
characterised by the presence of the Bundle of Kent, an accessory conducting pathway which is closer to the SA node than the AV node is. The atria are well-behaved, and they politely conduct the impulse from the SA node along the usual fast conduits. The P wave, therefore, is normal in appearance. Then, the impulse reaches the Bundle of Kent, and it conducts the impulse first, before the AV node has a chance
so PR interval short, delta wave (giving wide QRS)
oft get AF (can be hard to tell ireeg reg) or atrial flutter; 2 kinds of SVT, if the complexes are narrow, its orthodromic. If they are wide and with delta-waves, its antidromic; Orthodromic SVT in WPW can be treated much like any other SVT (adenosine, vagal manoeuvres etc), whereas in antidromic many drugs contra’d; VF also possible; the tachycardia from many of these rhythms can be fast enought for syncope and even sudden death
in orthodromic you block the AVN, no impulse transmitted, no V depol to re-enter, and the circuit is broken; narrow QRS
in antidromic, cycle goes other way from atria down accessory pathway into vents, then up AVN to atria to re-excite; theoretically safe to block AVN to terminate rhythm, but hard to be sure it is this and not AF with WPW as both give the broad QRS appearance so caution
caution bc AF waves transmitted into vent bounce crazily around the ventricle and create an electrical environment richly conducive to EADs, with some normal conduction down AVN hopefully creating a regular contraction and refractory period that controls the AF, so you block the AVN and lose this stabilising effect, giving VF
so adenosine, verapamil, digoxin, diltiazem no; procainamide yes, cardioversion yes; maintenance may be with flecainide if no structural heart disease, or eg sotalol if there is; accessory pathway ablation is an option
avrt (inc how to tell from avnrt)
trioventricular reentry tachycardia and Wolf-Parkinson-White syndrome are often used interchangeably. However, to be specific, AVRT is the most common type of arrhythmia associated with the Wolf Parkinson White syndrome
Atrioventricular Re-entry Tachycardia (AVRT) is a form of paroxysmal supraventricular tachycardia that occurs in patients with accessory pathways
In orthodromic AVRT, anterograde conduction is via the AV node, producing a regular narrow complex rhythm (in the absence of pre-existing bundle branch block)
In antidromic AVRT, anterograde conduction is via the accessory pathway (AP), producing a regular wide complex rhythm. This can be difficult to distinguish from ventricular tachycardia (VT)
Often triggered by premature atrial or premature ventricular beats
This rhythm can appear very similar to AVNRT, but the RP interval can assist us to differentiate:
In typical AVNRT, retrograde P waves occur early, so we either don’t see them (buried in QRS) or partially see them (pseudo R’ wave at terminal portion of QRS complex)
In AVRT, retrograde P waves occur later, with a long RP interval so see them as notch in p wave
patients that are unstable due to this rhythm require urgent DC cardioversion
otherwise vagal manouvres then adenosine/verpamil
generally accepted that intravenous administration of the calcium antagonist verapamil for the treatment of tachyarrhythmias is contraindicated in children under 1 year of age due to a proven risk of haemodynamic collapse and even death
for antidromic Procainamide (class I) would be our first line antiarrhythmic. Ibutilide (class III) and amiodarone are second-line options, but their effectiveness is less established, else DC cardioversion
avnrt (what it is, 5 reasons for it to happen, more common gender, how it presents (6 sx), difference physiologically from AVRT, why some ppl get AVNRT and how many have the potential to get it, how it looks on ECG (and what the most common subtype is), mx of acute episode, maintenance, definitive mx
Atrioventricular Nodal Reentrant Tachycardia is a type of SVT and is the commonest cause of palpitations in patients with hearts exhibiting no structurally abnormality
typically paroxysmal and may occur spontaneously in patients or upon provocation with exertion, coffee, tea or alcohol. It is more common in women than men (~75% of cases occurring in women) and may occur in young and healthy patients; sudden onset of rapid, regular palpitations. The patient may experience a brief fall in blood pressure causing presyncope or occasionally syncope.
If the patient has underlying coronary artery disease the patient may experience chest pain similar to angina
patient may complain of shortness of breath, anxiety and occasionally polyuria due to elevated atrial pressure releasing atrial natriuretic peptide
In comparison to AVRT, which involves an anatomical re-entry circuit (Bundle of Kent), in AVNRT there is a functional re-entry circuit within the AV node
AVNRT is caused by a reentry circuit in or around the AV node.
The circuit is formed by the creation of two pathways forming the re-entrant circuit, namely the slow and fast pathways. This is in ppl with AVN duality - 25-35% ppl have this
The fast pathway is usually anteriorly situated along septal portion of tricuspid annulus with the slow pathway situated posteriorly, close to the coronary sinus ostium.
If you have a sinus beat hitting the two strands- both strands conduct to ventricles, fast strand wins and ventricles aren’t ready for the slow strand anyway so it’s blocked= no problem! = Normal heart activity from atria to ventricle via AV node most of the time. But- If you then have an ectopic. The electrical wavefront will hit the slow strand which is already ready to conduct, but be blocked by the fast strand that isn’t ready. The electricity moves slowly down the slow strand and then reaches the bottom of the now reactivated fast strand, setting up a re-entrant circuit as it conducts to the atria up the fast strand
Slow-Fast AVNRT (Common AVNRT)
Accounts for 80-90% of AVNRT
retrograde P wave is obscured in the corresponding QRS or occurs at the end of the QRS complex as pseudo r’ or S waves
ECG:
P waves are often hidden – being embedded in the QRS complexes.
Pseudo r’ wave may be seen in V1
Pseudo S waves may be seen in leads II, III or aVF.
Generally at high rates this is typical SVT with no P waves
Patients may be instructed to undertake vagal manoeuvres upon the onset of symptoms which can be effective in stopping the AVNRT. This may involve carotid sinus massage or valsalva manoeuvres, which will both stimulate the vagus nerve. Alternative strategies include:
Adenosine, beta-blockers or calcium channel blockers can suppress an AVNRT event by blocking or slowing the AV node. Other second-line therapies may include amiodarone or flecainide.
Cardioversion is rarely used on patients with AVNRT, usually when the tachycardia is refractory to other medical therapies or the tachycardia is causing haemodynamic instability
BB +/- CCB for maintenance, esp in resource poor settings, and can consider catheter ablation for frequent attacks - eg cryotherapy of the slow path
pre-excitation syndromes
most common is WPW, covered in detail elsewhere
others include:
Lown-Ganong-Levine (LGL) Syndrome
Proposed pre-excitation syndrome. AP composed of James fibres.
PR interval < 120ms
Normal QRS morphology
Paroxysmal tachycardia
Mahaim-Type Pre-excitation
Right sided APs connecting either AV node to ventricles, fascicles to ventricles, or atria to fascicles
Sinus rhythm ECG may be normal, QRS may be wide as in WPW but PR interval will be normal
May result in variation in ventricular morphology
Re-entry tachycardia typically has LBBB morphology
vtach vs BBB with SVT; ecg + causes: left axis deviation in neonate, ASD, hypothermia, electrolyte imbalances, increased PR interval, digoxin
vtach may also be BBB with SVT (look for cannon waves in VT, also carotid sinus massage no effect in VT)
left axis deviation in neonate seen in av septal defect, tricupsid atresia, noonan syndrome
AD: ostium primum has left axis deviation and RBBB; ostium secundum has right axis deviation and RBBB
hypothermia: bradycardia, J wave hump in QRS, long QT, potentially v fib and shivering artefact
electrolyes: hypokal prolongs PR, depresses ST, inverts T waves, may have U waves; hyperkal peaks T waves, then p waves lost and QRS prolonged; hypocalc prolongs QT and hypercalc shortens it
PR interval increased by hypokal, myocarditis, rheumatic fever, ASD, ebstein anomaly, ischaemia, hypoxia, digoxin; PR decreased in WPW and ganong-levine syndrome
digoxin: prolonged PR and reversed tick ST segment depression, may see various arrhythmias inc ventricular bigeminy (alternating vent extrasytole and normal vent complex); hypokal makes toxicity more likely
paediatric SVT
SVT is the most common dysrhythmia seen in the paediatric population, and comprises over 90% of paediatric dysrhythmias. Of children presenting with SVT:
Half will have no underlying heart disease (esp in teens AVNRT is common and may have been triggered by exercise, stress etc)
1⁄4 will have WPW, Almost 1⁄4 will have congenital heart disease
Rapid, regular usually narrow (< 80 ms) complex tachycardia:
220 – 320 bpm in infants
150 – 250 bpm in older children (usually >220bpm)
P wave is usually invisible, or if visible is abnormal in axis and may precede or follow the QRS complex (retrograde P waves)
In contrast to sinus tachycardia does not respond to changes in temperature or fluid boluses and has no beat to beat variation
SVT may be well tolerated in infants for 12-24 hours. Congestive heart failure (tachycardia induced cardiomyopathy) later manifests with irritability, poor perfusion, pallor, poor feeding, and then rapid deterioration
Note that > 95% of wide complex tachycardias in paediatrics are not VT, but SVT with aberrancy:
SVT with BBB (in pre-existing congenital heart disease)
Accessory pathway re-entrant SVT
A 12-lead ECG in SVT and post-conversion is essential. Monitor with a rhythm strip during manoeuvres – this allows later assessment of underlying rhythm in unclear cases.
For any arrhythmia, treat fever & electrolytes (aim for iCa >1.0, K >4.0, Mg >1.0)
aim first to slow AV conduction:
Vagal manoeuvres
Infants: ice plus water in bag placed on face for up to 10 seconds – often effective
Older children: carotid sinus massage (some centres advise against this), valsalva manoeuvre (30 – 60 seconds), deep inspiration/cough/gag reflex, headstand
Adenosine
Causes transient AV nodal blockade, interrupting re-entry pathway through AV node
Half life < 10seconds
Side effects of flushing and bronchospasm are short-lived
Give 100mcg/kg rapidly into a large vein. Repeat after 2 minutes with 250mcg/kg
Maximum total dose 12mg
Be very wary of cardioverting an “unstable” child in SVT in ED who remains conscious to the point of requiring sedation or anaesthesia
Rapid deterioration of the “SVT-stressed” myocardium may occur with anaesthesia
If shock is present, synchronous DCCV is indicated at 1J/kg, repeat at 2 J/kg (monophasic)(give adenosine while setting up)
note subtype of automatic SVT:
SVT due to abnormal or accelerated normal automaticity (e.g sympathomimetics). Usually accelerate (‘warm up’) and decelerate (‘cool down’) gradually.
Sinus tachycardia: enhanced automatic rhythm. Rate varies with physiological state.
Atrial tachycardia: non-reciprocating or ectopic atrial tachycardia – rapid firing of a single focus in the atria. Slower heart rate (130-160)
Junctional ectopic tachycardia: difficult to treat, usually occurs in setting of post extensive atrial surgery. Rapid firing of a single focus in the AV node. Slower rhythm – 120-200bpm
WPW may be ortho or antidromic. If antidromic gives broad complex tachycardia, may be fast eg at ~280 bpm; could easily be mistaken for VT; however, remember that >95% of broad complex tachycardias in paediatrics are actually SVT with aberrancy (usually a re-entrant tachycardia)
Note if stable but resistant to adenosine (resists or restarts) discuss with paeds cardio, who may suggest:
amiodarone (good for ATACH), MgSO4 as adjunct to this, flecainide for WPW; rarely propanolol or verapamil
other paediatric arrhythmia
ATRIAL FLUTTER
Associations: Dilated right atrium, atrial surgery, digoxin overdose (more commonly seen in antenatal/postnatal period and rarer in kids)
technically a type of SVT, and may look like SVT until adenosine given when flutter waves will be revealed
treat like SVT stable and unstable, and discuss with paeds cardio
ENOSINE: rapid injection into large vein then immediate 10mL 0.9% sodium chloride flush using 3 way tap: onset instantaneous
Indication: Terminates some SVT. Aids identification of other arrhythmias (sinus tachycardia, atrial flutter, atrial fibrillation, VT).
Contraindicated in pre-excited AF (broad, irregular tachycardia)
Dosage: <12yrs: Start at 100 microgram/kg, ↑ by 100microgram/kg if no response to max 500 microgram/kg (neonates
resistant to lower doses) >12yrs: Start at 3mg, increased to 6mg then 12mg if no response.
ECG must be continuously recording (12 lead – if not possible then defib rhythm strip), mark when adenosine doses given
Side effects: BP, bronchospasm, sinus arrest, chest pain, tachycardia acceleration, treatment failure (see below)
Treatment Failure: If AV pause achieved but rhythm disturbance ongoing then further increased doses are unlikely to
cardiovert, consult a cardiologist for further advice
VTACH - note rare in kids, usually structural cause (congen or damage from eg myocarditis - cMRI can help look for this when stable)(despite this VTACH can kill, SVT rarely does, and so a wide QRS complex tachycardia should always be managed as VT until proven otherwise)
>4 broad complexes (PVCs) in succession will require treatment
Associations: Prolonged QT, CHD, anti-arrhythmic meds, tricyclic overdose (treat with sodium bicarbonate)
ECG: Wide, bizarre QRS complexes with AV dissociation
Management: ABC, general measures as above (including ventilation if shocked) and actively treat electrolyte abnormalities
CVS stable (with pulse) Magnesium sulphate 50-100mg/kg over 20 minutes (max dose 2g).
Discuss with cardiology Re: anti-arrhythmic medication: Amiodarone or lignocaine (latter may be preferred if evidence of long QT on previous ECGs)
Cardiology may consider use of adenosine if diagnosis unclear
CVS unstable (with pulse) Synchronised cardioversion 1J/kg, then synchronised 2J/kg. Add amiodarone if no response
bradycardia needs cardio discussion ?isoprenaline infusion or pacing
classifying SVT and VTACH vs SVT with aberrancy
regular atrial: sinus tachy, atrial tachy, atrial flutter, sinus node re-entry
regular AV: AVRT, AVNRT, automatic junctional
irregular atrial: a fib, flutter with variable block, multifocal ATACH
AVNRT is the commonest cause of palpitations in patients with structurally normal hearts - typically paroxysmal and may occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines)
sudden onset of rapid, regular palpitations +/- Presyncope or syncope due to a transient fall in blood pressure
Chest pain, especially in the context of underlying coronary artery disease
Dyspnoea
Anxiety
Rarely, polyuria due to elevated atrial pressures causing release of atrial natriuretic peptide
remember VT kills, so if unsure treat as that; also remember that in kids it is highly likely SVT with aberrancy
aberrancy could include bundle branch block, SVT with hyperkal/acidosis/NaV blockade as these all slow AP propogation, antidromic AVRT (WPW)
VT likelihood increased by: no BBB morphology, extreme axis deviation (northwest axis: QRS positive in aVR and negative in I and aVF), AV dissociation (P and QRS complexes at different rates), capture beats (Occur when the sinoatrial node transiently “captures” the ventricles in the midst of AV dissociation, producing a QRS complex of normal duration), fusion beats (occur when a sinus and ventricular beat coincide to produce a hybrid complex), taller left rabbit ear on RSR complex, notching near nadir of s wave
VT more likely clinically if >35yo, structural ir ischaemic heart disease, FH of HOCM/congen long QT/brugada syndrome etc
if really unsure can follow the brugada algorithm to differentiate the two
ventricular arrhythmia post-MI
There is a temporal distribution to VA post-acute MI: an early, or acute phase, of up to 48–72 hours, which is a time of very dynamic ischaemia and reperfusion. From 72 hours to a few weeks up to a month post event, and a more chronic phase beyond that, where remodelling continues to occur. Premature ventricular contractions (PVCs) are common in the early phase
Acute ischaemia causes hypoxia, which results in an intracellular depletion of adenosine triphosphate and the consequent accumulation of adenosine diphosphate and the products of anaerobic glycolysis, leading to intracellular acidosis. This drop in pH activates the Na+/H+ and Na+/Ca++ion exchange channels, with expulsion of hydrogen ions in exchange for sodium, which passes into the cell and is then exchanged for calcium, resulting in cell swelling and calcium overload. This is accompanied by the build-up of extracellular potassium, cathecholamines and lysophosphatidylcholine. This results in depolarisation of the cell membrane and reduction of the fast inward sodium current and increase in the late sodium current initially prolonging the action potential duration (APD). Ultimately, abbreviation of the APD, seen during ischaemia, results from decreased inward calcium currents (inhibited by the acidosis) and enhanced outward ATP-sensitive potassium current due to reduction in intracellular ATP
Spontaneous calcium oscillations trigger early and late after-depolarisation-induced ventricular ectopics
Surviving purkinje fibres with shortened APD or reduced amplitude, depolarised membrane potentials and reduced Vmax are thought to be the source of automatic foci for VA. The partial and temporal dispersal repolarisation contribute to a re-entrant mechanism based on regions of unidirectional conduction block; Tissue heterogeneity is particularly marked in the peri-infarct or ‘border zone’ and it is here that arrhythmogenesis is thought to arise and re-entry through a stable circuit involving the infarct scar tissue is the most-likely mechanism of sustained monomorphic ventricular tachycardia
palpitations (definition, 4 causes, clot risk in diff atrial rhythms, first of which has 10 lifestyle/medical subcauses, 6 ix)
awareness of ones own heartbeat, usually bc its stronger, faster, or more irregular than normal; disturbing for pt but not usually life threatening
inc awareness - generally no pathology, pt just becomes more aware of heartbeat due to relaxing or provoked by emotional upset, exercise, or eg alcohol, tobacco, ephedrine, caffeine, nicotine, cocaine, amphetamines, salbutamol; increased awareness of ectopics leads to feeling that heart skipped a beat and pts worry about thump of the relatively stronger next sinus beat
narrow complex tachycardia - eg psvt with HR 150-250bpm, lasting for seconds to days, regular; a fib has atrial rate up to 600bpm with av block giving irregular vent rhythm nonrelated to atrial rhythm; this can be paroxysmal; atrial flutter much less common with a rate up to 300bpm and variable conduction through av node giving slow vent response and saw toothed p waves; flutter atria beat regularly and vent may or may not, less clot risk; in afib atria beat irregularly and vent always irregular, more clot risk
panic attack - esp if pt more vigilant about heart disease due to recent heart problems with them or family; symptoms tend to peak within 10 mins; palps, sweating, shaking, sob or choking, chest pain, nausea, dizziness, derealisation or depersonalisation, fear of losing control, fear of dying, tingling or numbness in various places, chills or hot flushes
thyrotoxicosis - sinus tachy or a fib; palpitations usually will not be only symptom present
for arrhythmias, twenty four-seventy two hour ecg monitoring can be useful to identify type, pt keeps symptom diary over same time and can correlate the two; loop event recorders are another option; such monitoring should be done in any pt with clear history suggesting arrhythmia, plus tft, u&es, fbc, lfts; do an initial ecg on presentation
PVCs - ischaemia and mx, ways to reduce in healthy non ischaemic pt bothered by symptomatic PVCs, bigeminy
Sudden cardiac death (SCD) related to postmyocardial infarction (post-MI) occurs under conditions of ectopic triggers, reentrant ventricular tachycardia (VT), and ventricular fibrillation (VF). Frequent PVCs are indicators of poor prognosis in this respect.
Treatment includes correcting electrolyte abnormalities (hypokalemia, hypomagnesemia, hypercalcemia), improving respiratory status (hypercapnea, hypoxia), and in non-post MI healthy patients bother by symptomatic PVCs by treating hyperthyroidism, and avoiding medications that may precipitate ectopy such as digoxin, sympathomimetics, and tricyclic antidepressants. Avoidance of alcohol, amphetamines, caffeine, cocaine, and tobacco is also recommended
ventricular bigeminy is alternating sinus beat and PVC; driven by anxiety, caffeine, beta agonists, hypokal/hypomag, digoxin toxicity, ischaemia;; check U&Es, trop, do an echo, but if all okay then can d/c and advise less caffeine; can give beta blocker if symptomatic (also note other patterns like tri/quadrigeminy)
early after depolarisations (inc 4 causes)
secondary voltage depolarizations during the repolarizing phase of the action potential
EADs often occur when outward currents are reduced and/or inward currents are increased, resulting in the lengthening of action-potential as under these conditions, the L-type Ca channel (ICa,L) may reactivate and reverse repolarization during the AP plateau
4 causes: 1) A reduction of repolarizing potassium currents; (2) an increase in the availability of calcium current; (3) an increase in the sodium-calcium exchange current (INCx) caused by augmentation of Cai activity or upregulation of the INCx; and (4) an increase in late sodium current
benign early repolarisation (aka, what it looks like 4 features, who is it rare in, how to tell from pericarditis x5 ways)
aka high take-off
Widespread concave ST elevation, most prominent in the mid-to-left precordial leads (V2-5)
Notching or slurring at the J point
Prominent peaked, slightly asymmetrical T waves that are concordant with the QRS complex
No reciprocal ST depression
Up to 10-15% of ED patients presenting with chest pain will have BER on their ECG, making it a common diagnostic challenge for clinicians. BER is less common in patients over 50, and particularly rare in those over 70
Pericarditis can be difficult to differentiate from Benign Early Repolarisation (BER), as both conditions are associated with concave ST elevation. One useful trick to distinguish between these two entities is to look at the ST segment / T wave ratio and the Fish Hook Pattern
ST / T wave ratio of > 0.25 suggests pericarditis
ST / T wave ratio of < 0.25 suggests BER
Another clue that suggests BER is the presence of a notched or irregular J point: the so-called “fish hook” pattern
Also no PR depression and T wave not as tall in pericarditis, BER less generalised as tends to just be in precordial leads
