Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
522 Cards in this Set
- Front
- Back
|
what is the incidence of infective endocarditis in the US
|
10000-15000 each year
|
|
|
what percentage if infective endocarditis is in pts >60y
|
>50%
|
|
|
list some risk factors for infective endocarditis:
|
injecting drugs user
prosthetic heart valve structural heart disease degenerative valvular disease previous IE |
|
|
the highest mortality of Infective endocarditis is with which pathogens?
|
staph aueus or fungi
|
|
|
in what type of infective endocarditis is the lowest mortality?
|
that caused by strep viridans or in the case of early surgical intervention
|
|
|
what percentage of infective endocarditis is made up of streptococcal infection
and what is the larger strep bug to contribute to this? |
60-80%
Viridans; 30-40% |
|
|
list the streptococcal bugs that most commonly associated with infective endocarditis?
|
Viridans (30-40%)
enterococci (Strep like bug) (5-18%) others; beta haemolitic group A and group B (15-25%) |
|
|
what percentage of infective endocarditis is made up of staphylococci bugs?
what are they? |
20-35%
staph aureus (10-27%)- found in native valves most commonly and predominates in hospitalised pts and IVD users Coagulase negative (1-3%) |
|
|
what gram-neg aerobic bacilli are involved in infective endocarditis?
|
make up 1-13%
E coli Klebsiella HACEK |
|
|
what are the HACEK organisms?
|
Haemophilus
Actinobacilicus cardiobacterum hominis Eikenella corrodens Kingella |
|
|
where do gram neg bacilli infective endocarditis commonly occur?
|
in hospialized/instrumented patients
|
|
|
list the pathogens commonly invloved with native valve endocarditis:
|
Strep (55%)
Staph (30%) Enterococci (5-10%) |
|
|
what are the pathogens commonly assocaited with prosthetic valve endocarditis?
|
early on likely staph (50%); mostly coagulase negative staph such as s. epidermidis
Late staphylococci make up 30% |
|
|
what pathogen is commonly responsible for infective endocarditis in IVDUs
|
staph aueus
|
|
|
what is the major criteria for diagnosiing infecive endocarditis
|
1. positive blood culture
typical microorganism consistent iwith IE from 2 separate blod cultures; - viridans, strep bovis or HACEK ir staph aureus, enterococi or microorganism consistent with IE from persistenly postiive blod cultures defined as - 2 positieve blood cultures of samples drawn >12hours apart - all of 3 or a majority of 4 separate cultures of blood (firs and last sample drawn 1 hour apart) 2. Evidence of endocardial involvement postiive echo for IE showing: - oscillating inercardiac mass on valve - abcess - new partial dehiscence or prosthetic valve |
|
|
what is the minor criteria for infective endocarditis?
|
1. microbiological evidence:
- positive blood culture that does not meet major criteria serological evidecne of causative organisms; Bartonella heneslae (cat scratch disease), B quinana (in homeless men, acquired from flees), Chlamydophila psittaci, Q fever 2. immunological evidence - glomerulonephritis, some renal impairment with GN on biospy or at least red cell casts in urine - rheumatoid factors - Osler's nodes (not infective janeway lesions) - Rith spots; found on fundoscopy 3. Echo; consistent with IE but not meeting major criteria. |
|
|
describe the diagnostic/R approach to sub acute verus acute endocarditis?
|
subacute; ID of pathogen very important
Acute; immediate empirical trreatment with AB crucial for survival . |
|
|
list some additional/helpful investigations in infective endocardits?
|
ESR/CRP
normacytic anaemia urinalysis; red cell casts, haematuria, proteinuria or pyuria cryoglobulin hypocomplemntaemia false positive serological test for syphilis |
|
|
list 3 examples where you should assume infective endocarditis in a patient?
|
staph aurues bacteraemia
enterococcus faecalis bacteraemia viridans strep in >/= 2 blood cultures find unual gram neg - HACEK staph aureus acute meningitis polyarticular septic arthritis multple blood cultures with coagulase negative staph. |
|
|
what is a common cause of cultrue negative infective endocarditis?
|
Q fever.
|
|
|
why is Echo performed on all infective endocarditis pts?
|
to look for vegetations on the heart valves.
|
|
|
what is the preferred echo format for infective endocarditis
|
TOE is better that TTE
TTE senstitivty is ~60 and spec 90 TOE is 95 for both |
|
|
true or false
prosthetic valve endocarditis is more common in bioprosthetic than mechanical valves? |
false
the incidence is equal |
|
|
in prosthetic valve endocarditis which pathogen is common eary and which is common late?
|
early = epidermidis
late - aureus |
|
|
In which 4 circumstances is surgery recommended for infective endocarditis?
|
1. severe aortic/mitral regurgitation with progresive LV dysfucntion
2. valve dysfunction and heart vailure 3. mechanical complications; abscess or fistula 4. organism resistant to medical therapy |
|
|
when is surgery 'often' recommended in infective endocarditis?
|
1. There is an embolic event during medical treatment
2. there is a large (>10mm) mobile vegetation |
|
|
true or false
staph aureus in the urine of an uncatheterised febrile patient suggests an embolic lesion to the kidneys caused by infective endocarditis |
true
|
|
|
what is the empirical treatment for enteroccoci caused infective endocarditis?
|
beta lactam and an aminoglycoside (gentamycin)
|
|
|
when is surgery for infective endocarditis recommonded in the setting of a prosthetic valve
|
1. similar to native valve plus
2. para-valvular infection 3. valve dysfunction if progressive or severe. |
|
|
true or false
surgical outcomes in infective endocarditis are generally better than medical therapy alone if risk factors are present. |
true
|
|
|
true or false
regardless of risk factors the cumulative risk of CVD increases as a linear function until the age of 90 years |
true
|
|
|
what is an the standard for a normal lipid profile:
|
LDL <2.5
HDL>1 TG <2 (maybe <1.7) |
|
|
what does the evidence say about lowering lipids and risk for heart disease?
|
the lower the better.
studies show that LDL of <1.6 is better htan <2.4 demonstating our normal range is not giving us the lowest risk ratio. |
|
|
what is normal HDL for a woman
|
>1.1-1.2
|
|
|
which is the dominant source of cholesterol?
which has the strongest relationship with causing CVD |
LDL for both
the reverse is also true that lowering LDL has a strong protective factor |
|
|
true or false?
in the "prove it" study; they showed that agressive lowering of LDL (80mg atorvostatin0 leads to regression of atheroma while moderate treatment (40mg of pravostatin) actually makes atheroma worse. |
true - both reduce blood pressure (to different extents) however egressive treatment has addititve effects
|
|
|
for a 12% decrease in all causes of mortality how much would you need to decrease LDL cholesterol by?
|
1mmol/L
|
|
|
describe the relationship of TGs with HDL and LDL in the lipid profile
|
generally associated with low HDL and small LL particles.
|
|
|
in what people does the typical high TG profile occur in?
|
HDL <1 and TG >1.7 occurs in pts with metobolic syndromes, central adiposity, HTN and early onset diabetes.
|
|
|
have a TG level of greater than 1.2 increases your event rate by how much?
|
3 times
|
|
|
true or false;
because cholesterol levels modfiy the risk assocaited with TG they must be considere in the context of the whole profile. |
true.
|
|
|
who should we investigated cholesterol levels in?
|
all adults >20years
children with a FHx or premature CHD or familail hyperlipidaemia. |
|
|
what is the freidwwald formula of cholesterol?
|
LDL = TC - HDL - (TG/2.2)
this only apples when TG is <4 |
|
|
which is the particularly health group of fatty acids?
|
N 3 fatty acids; linolanic acid (plant drivative) and eicosapentanaenoic and docosahexanoic acids (fish derived)
|
|
|
what are some of the established effects of long chain polyunsaturated fatty acids
|
reduced plasma TG
imrpove endothelial function can elevate LDLs anti-inflammatory effects reduce platelet activity reduce plasma fibrinogen |
|
|
true or false:
circulating free fatty acid concentration predicts sudden death in asymptomatic men >22years |
true
|
|
|
true or false:
low red cell concentration of trans-isomers of linoleic acid and high concentrations of long chain n-3 fatty acids increase the risk of primary cardiac arrest |
FALSE
HIGH red cell ceoncentration of trans-isomers of linoleic acid and LOW concentrations of lng chain n-3 fatty asics increase the primary risk of cardiac arrest |
|
|
what are some nutritional changes shown to modify rish of a CV event?
|
Fish oil
mediterranear diet |
|
|
what are some causes of secondary hyperlipidaemia?
|
hyperthyroidism
diaeetes chornic renal failure nephrotic syndrome obstructive liver diease anaboic steroids |
|
|
describe the mechanism of action of statins in lowering lipid levels?
|
work on the liver by decreasing the production/synthesis --> upregulation of the LDL receptor to promost clearance of LDL
|
|
|
describe the mechanism of action of fibrates in lipid lowering:
|
Induce lipoprotein lipolysis; increase LDL removal and increase HDL producitno and reverse cholesterol transport.
they effect the enzyme actions; like lipoprotein protease; which clears/breaks down, hydrolises the TG to form remnants and this increases the synthesis of APO A1 in the liver. regulate metabolism of TG rich liopoproteins and can promote elevation of HDL indrectly becuase of TG metabolism effects. |
|
|
what is the mechanism of action of ezetimide
|
this is a cholesterol absorption inhibitor. this lowers LDL by blocing the uptake of it in the gut. has a 15-20% effect at lowering LDL. does not effect TG or HDL
|
|
|
name the most effective combination therapy for lipid lowering
|
Niacin (nicotinic acid) + statin + colestipol (bile acid binding resin) LDL lowering up to 60% and HDL raided by 13-20%
|
|
|
name the 2 combination therapies good at lowering TG as well as LDL and which is preferred
|
statin + niacin
STatin +fibrate Statin and niacin prefered becase with a fibrate there are more SEs |
|
|
what is the mechanism of bile acid binding resins in lipid lowering?
|
interrupt the enterohepatic bile acid circulation; they lower LDL by 20-30%, reduce VLDL and also raise HDL and TG
|
|
|
what is the mechanism of action of nicotinic acid in lipid lowering?
|
inhib lopoprotein seretion and decreases LDL by 15-25%, VLDL by 25-35% and raises HDL.
no effect on TG |
|
|
do fibrates have an effect on TG
|
yes tehy lower TG by 25-40%
|
|
|
what are the contraindications for recommending rish oil tablets
|
none.
ther are mild gasto issues and they are unpalatable however they are the safest thing to prescribe someone |
|
|
if LDL is the ony derragement in the pipid profile what would you prescirbe?
|
statin alone
if this is insufficient add niacin, BAS or exetimibe |
|
|
If LDL and TG are derranged in the lipid profile what would you prescribe?
|
statin in combination with a fibrate or fish oil
|
|
|
list some statin side effects
|
headache
myalgia faigue GI intolerance flu-like symptoms increased liver enzmes lyopathy |
|
|
what are some indications to cease a statin or not prescribe it
|
if there is preexisiting liver disease
a significant change in liver enzymes the presence of signifincant muscle toxicity |
|
|
what is one factor that contributes to the SE in statin use
|
polypharmacy. drug interactions causing increased intolerance can account for a significant proportin of side effects.
|
|
|
true or false
IF there are concerns of muscle damage simvastatin is the preferred statin agent |
false.
|
|
|
what drug do statins have the largest interaction with?
|
cyclosporin A
|
|
|
define a true aneurysm
|
dilatation of the artery to 2x the normal size with stretching and thinning of the wall and elongation of intact 3 layers of the vessel - intima, media and adventia
|
|
|
define a false aneurysm
|
usually secondary to trauma (may be endovascular precedure etc) contained rupture or anastamotic breakdown. Part of wall is made up of thickened fibrous material.
|
|
|
what is a mycotic aneurysm
|
this is rare
a bacterial or fungal infection; associated with bacterial endocarditis |
|
|
what is the width of the normal aorta
|
in males 21mm
in females 19mm |
|
|
in what percental of >65y are AAA's found
|
6-9%
and 4-6x more frequent in males |
|
|
at what point is a AAA clinically important
|
>5cm or if rapidly increasing in size
|
|
|
what are some common sites of aneurysm
|
abdominal aorta (most common)
aortoiliac - extension into the iliac arteries popliteal femoral aortic arch and descending thoracic aorta carotid *popliteal aneurysm is frewuently assoicated with AAA (~50%) |
|
|
what are some of the haemodynamic factors contributing to aneurysm formation?
|
HTN, flow divider, impedance mismatch
|
|
|
name some of the histologic patho-phyisology factors involved in arterial aneurysm
|
alterations in proteolytic enzymes - collagenase, elastase
activity of the aortic wall changes and the banace between breakdown and rebuilding of collegenasechanges; there is differene found in pts with ruptured versus no ruptured aneurysm |
|
|
what is the law of lapalace:
|
the tension in the wall is proprtion to the pressure times the raduis.
this means the greater the radius the greater the risk of rupture (na dah!) |
|
|
what are the RF for an aneurysm?
|
Smoking
FHx (1-5%) Ethnicity (northern europeans > asians, african) CAD Elevated lipids HTN Interestingly Diabetes is a protective factor because it causes stenosis |
|
|
what is the most common clinical presentation of a AAA
|
incidental finding on CT, US or MRI
|
|
|
what percentage of AAA are asymptomatic
|
75%
|
|
|
If found on examination how would a AAA present
|
pulsatile mass centred above or on the umbilicus; sometimes pts are obese and this will not be found on exam even if large
may also be signified by a distal embolus from thrombus rupture is a bad way to present. |
|
|
what are the 2 different ways a AAA can rupture and which has a worse prognosis.
|
intraperitoneal rupture; this has a high mortality becasue there is nothing to limit/contain the 3rd space blood loss
retroperitoneal; this is contained initially and thus give sa greater survival chance if get to theatre. |
|
|
what percentage of ruptured AAA survive?
|
50% - even if make it to surgery
|
|
|
what is the classic triad of the infra renal aneurysm rupture?
|
1. severe abdominal or back pain
2. pulsatile abdominal mass 3. shock |
|
|
what percentage of aneurysms are inflammatory?
|
5%
|
|
|
describe an infammatory aneurysm:
|
you will see a white thikening over the aorta
CT will shoud lumen, thrombus around it, wall of calcification around that, then thickein around the calcified outer wall that thickening is KEY to diagnosing infammatory aneurysm |
|
|
what was the key finding out of the UK small aneurysm trial and US veteran study
|
75% of surveillance group eventually came to surgery
61% of surveillance group came to surgery within 5 years there was no difference in oucomes for either group in both studeis |
|
|
what are the complications of an open AAA repair?
|
intraoperative haemorrhage
renal failure gut ischemia embolization wound infection/breakdown graft infection false aneurysm aortoenteric fistula MI lung collapse |
|
|
describve an endovascular aneurysm repair of AAA?
|
abdomen is not opened
delivered via groin graft is supported by stents have been used since 1991 |
|
|
what is a cook graft for AAA?
|
this is a bifurcaed flexible graft fixed with hooks in the AAA and iliac bifurcation
most successful one developed so far. shown to shirnk the old aneurysm sac over time. |
|
|
what is the selection criteria for a cook graft?
|
adequate neck: >15mm lenthm diameter <32mm, not excessively angulated
adequate access to vessels; size >8mm, not excessively tortuous and there are other anatomica criteria |
|
|
what is a type I endo leak of a AAA graft?
|
this is issues with the seal at either end, can be fixed with extension of the graft or ballon
|
|
|
what is a type II endoleak of a AAA graft?
|
commonly arising from the lumbar vessels or the inferior mesenteric arter --> bleeding into the seac even though the graft remains in tact and working
|
|
|
What is a type III endoleak of a AAA graft repair?
|
the graft join is disrupted
|
|
|
what is a type IV endoleak of a AAA graft repair?
|
the graft material is damaged, faulty or permeable (this was a problem of former grafts made of permeable material)
|
|
|
which type of endoleak most commonly leads to a post graft rupture of AAA?
|
type I endo leak.
|
|
|
in australia what is the averal size for intervention of a AAA?
|
51-60mm
|
|
|
what is a palpitation?
|
an unpleasant awareness of the beating of the heart
|
|
|
what are some common causes of palpitations
|
low CO
low arterial BP changes in cardiac chamber size venous distention |
|
|
how might a person experience or describe a ventricular ectopic beat
|
because of changes in the pressure in the ventricle due to incomplete filling, the patients sense missed beats which may be followed by a very large beat.
|
|
|
with regards to a ventricular ectopic beat what are some useful informations:
|
where atria and ventricles contract simultaneously; a large JVP wave is produced = lunp in the throat
|
|
|
what are some comomn associated symptoms to an arrhythmia
|
sweating, angina pectoris, presyncope, loss of consciousness
|
|
|
how long does a normal autonomic change in heart rate take compared with arrhythmia
|
arrhythmias are instantaneous; normal autonomic change takes ~30sec to com on and to go off.
|
|
|
describe retrograde amnesia in a patient suffering a cardiogenic blackout
|
when BP falls and the brain becomes ischemic there is a surge of autonomic activiy, but ptes then passes out; the longer they stay unconcious the greater the duration of the restrograde amnesia prior to the event; pts will report no memory of even feeling faint often. just the memory of walking followed by waking on the ground
|
|
|
what are some causes of a sudden drop in BP
|
postural, HTN treatment, bleeding, dehydration, autonomic dysfunction
|
|
|
in a person whose heart stops suddenly what is a key feature of their LOC event
|
as they pass out their eyes will first open widely and they will go pale, be agitated and within 15sec will pass out, they may develop convulsions if this goes on for a long time
autonomic activity wil resotre the beating of their heart and they face will dramatically flush pink. |
|
|
what particular murmurs are you listening for in a syspected arrhythmia
|
obstructive murmurs particularly so AS, MS, PS and pHTN
|
|
|
what is brugada syndrome?
|
recently described
ECG appearance leading to episodes of paroxysmal VT causing fainting. this is an ion chanel defect with a stong genetic factor good till 18y 50% dead at 50y |
|
|
what is a delta wave on ecg?
|
this is the sign of WPW syndrome. it is a blurring of the p wave with QRS upstroke. seen as an upstroke from the p wave to the complex
|
|
|
what is the immediate setting treatment for a clinically significant bradycardia
|
beta1 stimulating drugs; isopropel noradrenaline IV infusion 5mcg/min
|
|
|
what is the ST and LT management of a clinically significant bradyardia?
|
there is no drug treatment
ST treatment is catheterization for temporary pacing by external wire placement in the heart - but max of 2 weeks, <1week recommeded due to infection risk LT is pacemaker insertion |
|
|
describe a pacemaker:
|
it is plaed in ror above the pectoral muscle usualy of the left arm (due to right handedness)
the first lead travels through subclavian vein IVC and terminates in electrodes in the RV apex; this has the capacity to change the HR with changes in the vibration of the body. very good at emulating what a normal heart would do. the second lead terminates in the RA appendage, to pace the atria when too slow or sensing when aria fires and then synchronises ventricular contractions. More modern ones have a 3rd lead - travels to the coronary sinus and around onto the lateral wall of the LV in the cardiac vein, pacing LV at the same time as RV |
|
|
what is a common cause for a tachyarrhythmia
|
scarred myocardium --> reentry issues --> tachyarrhythmia
|
|
|
true or false:
a slow monomorphic VT (QRS all look the same) are usually harmless. extremely fast VT is often induced post MI and causes sudden death commonly |
FALSE
slower monomorphic VT are usually when pts have recurrent VT OR have it induced post MI and can lead to sudden cardic death fast VT usually not as deadly. |
|
|
are ventricular fibrillations dangerous?
|
can be part of normal physiology; not necessarily a higher risk of death or dysfunction.
|
|
|
describe an implantable defibrilltor:
|
has similar leads to a pacemaker but with longer electrodes able to administer high boltage shock; one is placed in the SVC and the other in the RV
the device tiself can be used as part o f the modification of the shock wave if required. |
|
|
is there effective medical treatment for arrhythmias?
|
no.
antiarrhythmic drugs are derivatives of quinidine or local anaesthetic drugs like lignocaine - usually found to actually be pro-arrhythmic - these drugs slow the conduction velocity more then they increase the refractory period, slow conduction acts to maintain/promote reentry loops --> arrhythmias |
|
|
when measuring blood pressure when is it that you use the 4th and not 5th phase to measure diastolic pressure
|
in a high output state such as pregnancy.
|
|
|
a normal cuff size measures
|
12x33cm
|
|
|
a thich cuff size measures
|
18x36cm
|
|
|
what is the definition of high BP
|
>140/90
|
|
|
is there a benefit to lowering BP below HTN level
|
yes. studies demonstrate that like cholesterol and weight the lower it goes the more benefit there is to reducing risk of a cardiovascular event
this is particularly true to high risk patients with 'normal' BP |
|
|
markedly increased BP at >180/100 is also known as
|
malignant HTN
|
|
|
list the four areas of serious complications in very high blood pressure
|
heart failure
renail failure encephalopathy papoloedema |
|
|
what are some of the "other" complications that managing extremely high HTN is trying to avoid?
|
acute intracellular haemorrhage
pre-eclampsia, aortic dissection, epistaxis |
|
|
what percentage of australians have high blood pressure
|
20% above 140/90
higher prevalence with age |
|
|
what are some of the factors affecting/modulating essential HTN
|
EtOH
high salt diet caffeine weight fitness/lifestyle hyperlipidaemia |
|
|
what are some adrenal causes of secondary HTN
|
primary hyperaldosteronism
Cushing's disease Phaechromocytoma abnomal corticosteroid metabolism |
|
|
describe a phaeochromocytoma briefly
|
occur in the adrenal gland and secrete adrenaline or adrenaline like substances however 10% do not occur in the adrenal gland
24h urinary catecholamine is the diagnostic test; require 3 negative to rule out |
|
|
what are some iatrogenic causes of secondary HTN
|
OCP
steroids carbenoxolon liquirice MAO inhibitors |
|
|
what are some signs to look for on examination of a pts first presenting with HTN
|
palpable kidney, oedema, abdominal bruit, delated femoral pulses, cushing's/acromegaly signs, cafe au lait patches, neurofibromata, orthostatic hypotension, uraemic features
|
|
|
list the investigations performed on ALL hypertensive pts
|
urinalysis and kidney function
renal ultrasound ECG and echo |
|
|
list some further investigations that may be considered in the hypertensive pt
|
formal renal testing
IVP, RPG, MCU renal angiogram PRA/aldosterone, Na balance Cortisol levels catecholamines |
|
|
ridged ribs on a CXR could indicate what crdiovascular disease
|
this is a sign of the aorta causing HTN in the arms and sometimes underdevelopment of the lower body.
the rib notching is caused by collaterals in teh chest wall that are larger than they should be causing frictional errosion. |
|
|
what is the first line treament of essential HTN
|
most recently it has been ACEi/ARBs however for some elderly pts first line is still often a thiazide diuretic
|
|
|
In what conditions are ACEi prefered?
|
diabetes,
kidney disease especially proteinuria heart failure they also work well in combination with CCB or diuretic |
|
|
name 3 dihydropyridine CCBs
|
nifedipine
amlodipine and felodipine |
|
|
name 2 non-dihydropyridine CCbs
|
verapamil
diltiazem |
|
|
what is the mechanism of action of a DHP CCB?
|
peripheral vasodiation; it is effective and powerful
SE oesdema, headache, constipation, flushing |
|
|
what is the mechanism of action of non-DHP CCBs?
|
act both centrally and peripherally.
there is some perihpheal vasodilatory effects also has direct negative ionotropic effect on the heart - Use with EXTREME caution with beta-blockers if at all. |
|
|
what are the main SE related to beta-blockers;
|
bradycardia
bronchospasm lethargy impotence |
|
|
anes some 'other' less common agents used to treat HTN
|
renin inhibitors
prazosin nethyldopa |
|
|
for people with chronic kidney disease or diabetes what is the target BP range
|
<130-85
|
|
|
what size vessels does atherosclerosis affect
|
large and medium sized muscular arteries
|
|
|
what are the characteristic mechanisms in atherosclerotic disease
|
endothelial dysfunction
vascular inflammtion and the build up of atheroma |
|
|
what are the key risk factors in atherosclerosis
|
age >40
male non-cacasian cigarette smoking* diabetes* HTN dyslipidaemia hyperhomocysteinaemia phyiscal inactivity HIV+ and on HAART chronic haemodyalysis |
|
|
describe the pathology of atherosclerosis
|
lipid in the arterial intima - fatty streaks
lipid peroxidation signal adhesion molecule expression on the endothelium monocyte adhesion monocyte -->macrohpage smooth msuce cells from the media enter the plaque and participate in cap formation plaque accumulates hydroxyapatitte mineral - calcifies matrix metalloproteinase accumultes in lesion --> rupture potential |
|
|
describe an unstable plaque in atherosclerotic disease
|
many foam cells + the extracellular matric sparating the lesion fro the arterial lmen is usualy weak and prone to rupture
|
|
|
what are 2 key findings on examination for hyperlipidaemia
|
xnthelasma and tendon xanthomata
|
|
|
what are some key findings on examination for peripheral vascular disease
|
decreased peripheral pulses
peripheral arterial bruits pallor peripheral cyanosis gangrene and ulceration |
|
|
what is a normal lipid profile
|
LDL <2.5; HDL >1 and TG <1.7
|
|
|
what is the standard treatment for high cholesterol
|
statins
|
|
|
name 4 statins
|
atorvostatin
fluvastatin pravastatin rosuvastatin simvastatin |
|
|
summarise stable angina
|
fixed stenosis
demand related ischemia that is predictable risk assessed by exercise testing |
|
|
summarise unstable angina
|
dynamic stenosis
supply related ischemia, can occur at rest and is unpredictable risk assessed by; frequency, nocturnal, other symptoms, ECG and troponins. |
|
|
what are some RF/triggers of angina separate from the RF of atherosclerosis?
|
exercise
mental stress sexual activity tachycardia; any cause metaboli; fever, thyrotoxicosis and hypoglycaemia |
|
|
describe the early path of angina briefly
|
without collateral coronary circulaion; at a stenosi of >70% the patient will start to experience angina related the demand mediated ischemia
|
|
|
describe the ongoing pathology of angina:
|
Oxygen demand increases; HR, BP and myocardiacontractability all effected --> LV hypertophy
oxygen supply affected; duration of diastole coronary perfusion pressure, coronary vasomotor tone, Hb |
|
|
what are some examples of atypical preenttion of ischemic heart disease
|
pain in the epigastrium
pain in the jaw alone pain in the neck or arms alone light headedness silent ischmia - common in diabetics |
|
|
what are the 4 key primary investigations in ischemic heart diease
|
ECG
Hb Fasting lipids Fasting blood sugars |
|
|
what are some reasons to terminate an excercise stress test in a pts with ischemic heart disease
|
sBP drops >10mmHg from base line
mod-severe angina experienced sings of poor perfusion sustained VT ST elevation w/out diagnositic Q wave |
|
|
how is a stress echocardiogram performed
|
images taken of the heart before exerise and then 60-90sec after
|
|
|
what is a positive stress echo?
|
stress inducing decreased regional wall motion, decreased wall thickening or regional compensaory hyperkinesis
|
|
|
what is the inital medical treatment for ischemiac heart disease - angina
|
GTN spray 400mg 5min interval maximum 3 doses
GTN tablet subligual as above isosorbide dinitrate 5mg sublingually as above (for pts with adverse reaction to GTN |
|
|
what are some further treatments for ischemic heart disease
|
antiplatelet therapy; low dose aspirin 75-300mg
beta blocker; reduces the myocardial oxygen demand - atenolol 25-100mg/day nonDHP CCBs; reduces HR and can be an alternative to Beta-blocker statins for cholesterol |
|
|
what is treatment following a coronary angiography proceedure?
|
aspirin indefinately
clopidergrel; recommended 6 weeks after bare metal stent and at least 12months after drug eluting |
|
|
list some adverse prognostic markers in a pts with unstale angina
|
pain at rest
signs of LV failure ST depression on ECG |
|
|
What percentage of acute coronary synrome presentation is accounted for by MI with no ST elevation
|
2/3
|
|
|
list the medications used to treat acute coronary syndrome
|
O2, Aspirin + clopidegrel, morphine
GTN Beta blockers; targeted to a H of 50-60bpm nitrates used if brta-blocker is ineffectlve CCB if beta blocker inefective ACEi and statin for comorbid conditions revascularisaion surgery |
|
|
what is the risk of death after from MI if acute coronary sydnrome is untreated
|
5% per year
after first MI 10% per yer |
|
|
what is the defintion of a STEMI
|
acute thrombotic occlusion of a coronary artery casuing MI and ST elevation on SCG findings
|
|
|
what percentage of ACS is accounted for by STEMI
|
25%
|
|
|
what percentage of pts with STEMI have evidene of coronary thrombus occluding the infarct artery
|
90%
|
|
|
in a STEMI: at the site of a ruptured plaque a platelt monolayer forms; which agonists promote the platelet activation?
|
collagen exposure
ADP epinephrine 5HT |
|
|
in STEMI: at the site of thrombus formation where flow is interrupted what is released and what is the effect?
|
thromboxane A2 is released and it is a potent local vasoconstrictor
|
|
|
what is the consequence of a persistent severe occlusion to a coronary artery?
|
myocardial cell necrosis
|
|
|
in STEMI was heart sound is an important sign to listen for?
|
additional sound S4
|
|
|
the ECG of a STEMI requires
|
persisitent ST elevation in 2 or more anatomical contiguous leads in the context of a consistent clincal history.
OR left bundle branch block |
|
|
Left bundle branch block is seen in an ECG as:
|
QRS complex >0.12s in limb leads
no Q wave in leads I, aVL and V6 slurred R in V6, absent Q and depressed ST with intereted T. tall R in V6 and bload slurred R in I and avI |
|
|
serial troponins are taken at what times
|
0hr
6-9hr, 12-24hr |
|
|
what is the pattern of CK rise in STEMI?
|
rises at 4-8hours and returns to normal 48-72hour
|
|
|
CKMB is more or less specific for MI?
|
nore specific for cardiac tissue damamge.
CkMB: CK >2.5 suggestive of a cardiac cause. not MI necessarily. |
|
|
what is the immediate treatment of STEMI
|
stabilise and rescusitate and then revascularisation with PCI, thrombolytics (if within 90minutes)
|
|
|
what are some pharmacological managemt options in STEMI
|
aspirin is used in the initial phase of a STEMI
glycoprotein inhibitors appear to be used for preventing thrombotic complications when undergoing PCI acute intravenous beta blockade improves myocardial oxygen supply and decerases incidence of ventricular arrhythmia ACEi |
|
|
why/how are beta blockers used in the treatment of a presenting STEMI
|
IV beta blockade improves myocardiac oxygen supply and decreaes the incidence of ventricular arrhythmias
|
|
|
why/how are ACEi used in the treament of a prsenting STEMI
|
the michanism involes a redution in ventricular remodelling after infarction
|
|
|
what is the 30 day mortality of AMI?
|
30%
|
|
|
what is the rate of sudden death in a post MI pt
|
4-6x greater than the non MI population
|
|
|
what is the rate of in hospital death and re-infarction post MI
|
5-10%
|
|
|
what is aortic dessection?
|
A separation in the aortic wall intima leading to blood flow into a new false channel composed of an inner and pter layer of the media
|
|
|
what is the ratio of men to women in aortic dissection
|
2:1
|
|
|
when is the peak age for aortic dissection
|
age is arisk factor but peak incidence is 60-80y
|
|
|
what are some comorbid RFs for aortic dissection
|
marfan's syndrome
cystic medial necrosis HTN ahterosclerosis takayasu's arteritis giant cell arteritis Bicuspid aortic valve aortic coarctation T3 of pregnanc |
|
|
what is a key histological predisposing factor to aortic dissection?
|
any condition that interferes iwth the normal integrity of the elastic or muscular components of the medial layer can predispose to aortic dissection
|
|
|
in aortic disection what does the intimal tear lead to
|
degredation of the medial layer of the aortic wall
|
|
|
which type of tear is more common in aortic disection?
|
circumferential is more common that transverse
|
|
|
where is acommon site for aortic dissection
|
often in the right lateral wall of th ascending aorta
|
|
|
the pulsatile aortic flow causes what in ortic dissection
|
--> dissects the elastic lamellar plates of the aorta and creates a false lumen --> blood thorugh the media most commonly proximally
|
|
|
in an aortic dissection; as it propogates what can occur?
|
there can be occlusion of flow through the branches of the aorta including the coronary, brachicephalic, intercostal, visceral and renal or iliac vessels.
|
|
|
what does secondary distal intimal disruption in aortic dissection lead to?
|
reenty of blood from the false to true lumen
|
|
|
in the stanford classification of aortic dissection what is a Type A:
|
involves the ascending aorta independent of the site of the teat - this is common ~65%
|
|
|
what is a stanford classification type B aortic dissection?
|
invoves the transvser and or descending aorta without involvement of the ascending aorta.
|
|
|
what is the presentation of an aortic dissection
|
pain; tearing, very abrupt onset, collapse is common
|
|
|
in aortic dissection of the ascending aorta where is the pain located?
|
anterior chest
|
|
|
in an aortic dissection of the descending aorta where is the pain located?
|
intra capsular
|
|
|
what are some common signs and symptoms of aortic dissection
|
HTN
asymmetry of brachial, carotid or femoral pulses signs of aortic regurgitation left pleural effusion |
|
|
match the complication to the following occluded vessels in aortic dissection:
coronary carotid spinal caeliac/sup mesenteric renal limb vessels |
MI
stroke paraplesia infarction with acute abdomen renal failure acute limb ischemia |
|
|
what are some possbile ECG findings in aortic dissection
|
ST depresssion, (elevation rare)
signs of LV hypertrophy in HTN or inferior MI |
|
|
will aortic dissection yeild positive cardiac enzymes
|
no
|
|
|
what is the CXR finding in aortic dissection
|
braodening of the upper mediastinum and distortion of the aortic 'knuckle' - 90%
|
|
|
what will be seen on a doppler echo in aortic dissection
|
aortic regurg, dilated aortic root and flap of aorta
|
|
|
what is the treatment for a type A aortic dissection
|
emergency surgery to replce ascending aorta
|
|
|
what is the treatment for a type B aortic dissection
|
treated medically unless there is actual or impending external rupture or organ/im ischemia
|
|
|
what is the medical managment for aortic dissection?
|
maintain MAP at 60-70mmHg using B-blocker, CCB, Na nitroprusside
|
|
|
what is the in hospital mortality rate of medically treated type B aortic dissection
|
10-20%
|
|
|
what is the surgical treatment for aortic dissection?
what if the aortic valve is invloved? |
excision of the intimal flap, obliteration of the false lumen and placement of an interpostion graft
a composite valve-graft conduit is used if the aortic valve is disrupted |
|
|
in a AAA what infectious agents are assocaited with a mycotic aneurysm?
|
rare; staph and salmonella
common; chlamydophila pneumoniae |
|
|
what is the proposed aetiology of an inflammatory AAA?
|
disproportionate proteolytic enxyme acitivty promoting deterioration of the structural matrix proteins (elastin and collagen) in the media and adventitia
|
|
|
is antibiotic care indicated for a pt undergoing AAA repair?
|
yes - must cover gram positive and gram negative
|
|
|
what is Aortitis?
|
it is a vasculitis syndrome; inflammation of the aorta, representing a cluster of large-vessel disease with unknown aetiology
|
|
|
what are RF for Aortitis?
|
female (9:1)
aged 10-40 connective tissue disorder e.g., SLE, RA, ankylosiing spondylitis, giant cell arteritis, reiter's syndrome, takayasu's disease |
|
|
In Aortitis what are the common infectious agent causes?
|
Neissera
tuberculosis Rickettsia sp. spirochetes (e.g., syphilis) fungi viruses (herpes, varicella) |
|
|
what is takayasu's disease?
|
this is a chronic vasculitis that targets the aorta and its major branches.
80-90% are women onset 10-40y |
|
|
how would a pt with takayasu's disease typically present
|
malaise and fever
some focal Sx related to inflam of vessel incl. cerebrovascular ishcemia, MI arm claudication or HTN |
|
|
In Aortitis what pathology occurs in the Intima
|
mucopolysccharides accumulate and thicken
|
|
|
in aortitis what pathology occurs in the media and adventitia
|
mixed cellularity infiltration with granuloma and gimant cells
|
|
|
what is Phase I of Aortitis
|
pre-pulseless inflammaotry preiod characterised by non-specific systemic symptoms, including low grade fever, fatigue, arthralgia and weight loss
|
|
|
what is phase II of Aortitis
|
involves vascular infalmmation associated with pain (e.g., carotidynia) and tenderness over the arteries
|
|
|
what is phase III of Aortitis
|
the fibrotic stage
with predominant ischemic symptoms and signs secondary to dilatation, narrowing or occlusion of the proximal or distal branches of the aorta |
|
|
In aortitis dilatation of the aorta leads to what?
|
Aortic insufficiency
|
|
|
In Aorititis what is the end result in the major branches of the aorta?
|
fibrous thickening and ostial stenosis
|
|
|
in aortitis ostial stenosis and fibrous thickening cause what?
|
reduced of absent pulse
low BP in arms centra HTN due to renal artery stenosis ocular disturbances neurological defects claudications |
|
|
what percentage of pts with Aortitis will have central HTN?
|
33-76%
|
|
|
what are some of the possible treatments for Aortitis?
|
presnisone +/- immunosuppresion with cyclophosphamide
anti-TNF (etanercept, Infliximab) antibiotics surgical bypass maybe helpful in some cases |
|
|
what are the 4 main complications of Aortitis
|
takayasu's retinopathy
HTN aortic regurgitation aneurysm |
|
|
what is a dilated cardiomyopathy?
|
characterised by dilatation and impaired contraction of the left ventrical; LV mass increases but wall thickness is normal or reduced
|
|
|
what is a hypertrophic cardiomyopathy?
|
characterised by inappropriate and elaborate LV hypertrophy with misalignment of myocardial fibres
|
|
|
What is Restrictive cardiomyopathy?
|
this is very rare and is when ventricular filling is impaired because the ventricles are stiff. Charactersied by abnormal diastolic function, often with mildly decreased contractabliity and ejection fraction (30-50%)
|
|
|
what are the RF for dilated cardiomyopathy?
|
>25% due to genetic AD inheritance
single mutations Id'ed affecting proteins in cytoskeleton of myocyte EtOH autoimmune reaction of viral myocariditis chemotherapy drugs (anthracyclines) male |
|
|
which is the most common type of cardiomyopathy?
|
hyperrtrophic (1/500-1000)
|
|
|
what are the risk factors for hypertrophic cardiomyopathy
|
1/2 due to degree of geentic penetration and vaiable gene expression
occurs in 20-40yr |
|
|
list the known genetic mutations in hypertrophic cardiomyopathy
|
single point mutation; encode sarcomere contractile protiens
beta-myosin heavy chan mutations assocaited with elaborate ventricular hypertrophy troponin mutation assocaitei with little or sometimes no hypertrophy but marked myocardial fibre dissaray - high risk of sudden death myosin-binding protein C mutation - presents later in life |
|
|
what are some of the risk factors for restrictive cardiomyopathy?
|
infitrative amyloidosis
mostly caused by amyloidosis caused by abnormal production of Ig ligh changes familial amyloidosis is AB mutation in transthyretin fibrotic endomyocardial idiopathic storage related - in myocytes |
|
|
what is takatsubo's cardiomypathy
|
atypical ballooning, or stress induced, cardiomyopathy
typically occuring in older women after an intensly stressful event resolves spontaneously no proven treatment |
|
|
what is the pathophys of takatsubo's cardiomyopathy?
|
ventricles show global dilatation with basal contraction
LV dysfunction will extend beyond a specific coronary artery distribution and generally resolve within days to weeks. may recur |
|
|
how does takatsubo's cardiomyopathy present?
|
pulmonary oedema
hypotension chest pain - ECG mimic acite MI |
|
|
what are the pathological findings in a dilated cardiomyopathy?
|
injury--> cardiac myocyte death -->surviving monocytes hypertrophy from wall stress burden --> MR develops
Histology myofibrillary loss interstital fibrosis Tcell infiltration |
|
|
what are the pathological findings of a hypertrophied cardiomyopathy
|
disordered myocyte architecture with swirling branches and branching rather than the usual parallel arrangement of myocyte fibres
myocyte nuclei vary markedly and interstitial fibrosis is usualy present. |
|
|
what is the pathological findings of restrictive cardiomyopathy?
|
amyloid fibrils infitrate the myocardium
this is especially in the conducting system and coronary vessels conduction block, autonomic neuropathy usually renal involvement too both atria and ventricles are affected |
|
|
which symptoms of a cardiomyopathy particularly occurs in the young?
|
peripheral oedema
|
|
|
true or false
all three types of cardiomyopathy can be associated with atrioventricular valve regurgitation |
true
because the structure and movement of the heart is the primary pathology not a valve pathology. |
|
|
what is the ejection fraction in a dilate cardiomyopathy?
|
>35 - when symptoms are severe
|
|
|
what is the ejection fraction in a hypertrophic cardiomyopathy?
|
>60%
|
|
|
what is the ejection fraction in a restictive cardiomyopathy?
|
25-50%
|
|
|
what is the LV diastolic dimension in a dilated cardiomyopathy?
(normal is <55mm) |
>60mm
|
|
|
what is the LV diastolic dimension in a restictive cardiomyopathy?
(normal is <55mm) |
>60mm
|
|
|
what is the LV diastolic dimension of a hypertrophic cardiomyopathy? (normal is <55mm)
|
often this is decreased
|
|
|
what is the atrial size like in cardiomyopathies
|
increased
in restrictive it is often massive |
|
|
what is the commonest first symptom presentation of:
dilated- restrictive- hypertrophic- cardiomyopathies |
exertional intolerance
exertional intolerance + fluid retention exertional intolerance +/- chest pain |
|
|
what arrhythmia's are related to
dilated- restrictive- hypertrophic- cardiomyopathy |
VT, conduction block in Chagas disease, AF
AF (ventricular arrhythmia uncommon) VT and AF |
|
|
when there is increased LV pressure what might be heard on auscultation
|
S4 gallop
|
|
|
when there is increased LV volume what might be heard on auscultation?
|
S3 gallop
|
|
|
what respiratory sign is likely in cardiomyopathy
|
crackles in the lungs - pulm congestion
|
|
|
what is the use of ECG in cardiomyopathy investigation
|
98% negative predictive value when systolic dysfunction is suspected
|
|
|
can an ECG diagnose dilated cardiomyopathy?
|
no - there will be non-specific chages Echo is required for diagnosis
|
|
|
what might an ECG show in hypertrophic cardiomyopathy?
|
pseudo infarct or deep T wave - showing LV hypertrophy and Q waves
Echo is diagnostic though |
|
|
what is the treatment for dilated cardiomyopathy?
|
controlling the resulting heart failure, use beta-blockers and ARBs. ?implantable defib?
|
|
|
what is the treatment for hypertrophic cardiomyopathy
|
symptom management and prevention of sudden death
beta blockers and nonDHP CCBs (e.g., verapamil) arrhythmia may respond to amioderone consider implantable defib for pts at risk of sudden death outflow tract obstruction may be surgically resected septal ablation may be necessary digoxin and vasodilators also used to treat increased outflow obstruction but AVOID |
|
|
what is a sinus arrhthmia?
|
normal
inspiration accellerating HR result of norma PSNS acitivty |
|
|
what is a sinus bradycardia?
|
regular and <60bpm at resy
|
|
|
with regard to the heart, what is automaticity?
|
spontaneous diastolic depolarisation.
the ability of the cell to depolarise itself to threshold. |
|
|
which cells in the heart have automaticity/
|
the SA node, the AV node, the His-Pukinje system, teh coronary sinus and the pulmonary veins
|
|
|
with regard to the heart what does 'triggered activity" mean?
|
abnormla depolarization occurinf during or after repolarisation. Oscillations of membrane predisposing factors.
this is a posulated mechanism of torsade de pointes |
|
|
what is a re-entry with regards to heart conduction
|
parallel electrical circuit with differnt refractory period
|
|
|
list 3 bardyarrythmias?
|
sinus bardyarrythma
sinus arrest escape rythms (junctional or ventricular) |
|
|
name 4 conduction delay types:
|
1. AV nodal conduciton blocks
2. primary,secondary, tertiary 3. fasciular 4. bundle branch blocks |
|
|
what are some narrow complex arrhythmias?
|
SVT
Atrial flutter AVNRT WPW |
|
|
name 2 wide compled arrhythmias?
|
SVT with aberrancy (for BBB)
ventricular tachyardia |
|
|
what are some RF for cardiac arrhthmias?
|
large left atria (AF)
bradicardia hypoxia or acidosis electrolyte disturbance myocarditis, infective endocarditis cardiomyopathies ischemia increased sympathetic tine |
|
|
what is cardic arrest/exit block?
|
sinus node stops firing or depolarizing fails to exit the S node. Escape beats may develop.
|
|
|
what is a single chamber pacemaker?
|
1 pacing lead in the RA or RV
|
|
|
what is a dual chamber pacemaker?
|
2 pacing leads are implantable in the RA and RV
|
|
|
what is biventricular pacing?
|
cardiac resynchronization therapy
single or dual chamber right heart pacing leads and a lead in the coronary sinus for the LV epicardial pacing |
|
|
describe the SA node
|
is composed of a clusdter of small fusiform cells located in the sulcus terminalis on the epicardial surface at the RA-superior vena caval junction; they envelop the the SA nodal artery
|
|
|
what is type I seconda degree SA block?
|
results from progressive prolongation of the SA node conduction and appears on the ECG as a progressive lengthening of the P-R interval and progressive shortening of the R-R interval, followed by a pause.
|
|
|
what is type II second degree SA block?
|
there is no change in the PR interval before the pause occurs (unlike type I with progressive lengthening of PR)
|
|
|
what is type III (complete) or third degree SA block?
|
no P waves on ECG
|
|
|
what are some extrinsic causes of SA block/sick sinus syndrome?
|
autonomic; carotid dinus hypersensitivity, vasovagal (cardioinhibitory stimulation
drugs; beta-blockers, CCB, adenosine, lithium, cometidine, anitriptyline. hypothyroidism sleep apnoea, hypoxia hypothermia, ICP |
|
|
What are some intrinsic causes of SA block/sick sinus syndrome?
|
CAD
inflam: pericarditis, myocarditis, Rheumatic heart disease, lyme disease senile amyloidosis radiation therapy genetic; AD Sick sinus syndrome, kearns-Sayre syndrome Myotonic dystrophy fredrich's ataxia |
|
|
true all false
all untreated pts with develop SVT |
false
25-50% of pts with SA block will develop an SVT - usually AF or Atrial flutter. |
|
|
what is the treatment for SA block?
|
symptom management and possible insertion of implantable pacemaker.
|
|
|
what is atrial flutter?
|
Large reentry circuit usually in the RA encircling the tricuspid annulus
atrial rate will be around 300bpm |
|
|
what is atrial flutter associated with?
|
2:1, 3:1 and 4:1 AV block
HR is 150, 100 or 75 respectively |
|
|
what is the name of the atrial flutter ECG
|
saw toothed
|
|
|
it might be difficult to see flutter waves if there is 2:1 block so....
|
apply carotid sinus pressire or IV adenosine --> will induce temporary AV block and reveal flutter waves
|
|
|
what is the treatment for Atrial Flutter?
|
digoxin
beta-blocker verapamil all used to control rate may need to restore sinus rhythm bia direct cardioversion or IV amioderone Catheter ablation offers 90% change or complete cure |
|
|
what is the most common cardiac arhthymia?
|
AF
|
|
|
what is AF?
|
abnormal automatic firing and multiple interacting renetry circuits looping round the atria
|
|
|
what is the effect of AF in the heart?
|
the atria beat rapidly in an uncoordinated manner --> this is ineffective
the ventricles are activated irregularly there are often ectopic beats (from the pulmonary vein) and these are sustained by re-entry within the atria |
|
|
what are the RF for AF?
|
age
enlarged atria underlying pathology that distrupts atrial conduction |
|
|
what are the causes of AF?
|
CAD, AMI, valvular disease, HTN< SA disease, Hyperthyroidism, EtOH , cardiomyopathy, congenital heart disase, chest infection, PE, Pericardial disease, Idopathic
|
|
|
what is the clinical presentation of AF
|
Palpitations, SOB and fatigue
it is often asymptomatic |
|
|
what are the 3 classifications of AF?
|
paroxysmal (intermittentand self limiting)
persistent (prolonged episodes terminated by cardioversion) permanent (cardiovesion fails) |
|
|
what is the treatment for paroxysma AF?
|
1st beta blocker
2 class Ic drugs propafenon, flexanide (never with CAD or Lv dysfunction) 3 amioderone 4 catheter ablation |
|
|
which drug treatments are not effective in AF?
|
digoxin and verapamil
|
|
|
what is the treatment for persistent+ AF?
|
attempt restoratin
1 digoxin 2 add beta blocker, verapamil or diltiazem may need to implant a pacemaker |
|
|
what is the success rate of cardioversion in AF?
|
75% success but 70-90% revert within a year
|
|
|
what is first degree atrioventricular block?
|
prolongation of the PR interval on ECG (>200ms)
|
|
|
what is 2nd degree AV block?
|
atrial impulses (generally occuring at a regular rate) that fail to conduct to ventricles in 1 of 4 ways (Mobitx classification)
|
|
|
what is a Mobitz I second degree AV block also called
|
Wenchebak block
|
|
|
what is a Mobitz I second degree AV block?
|
progressive prolongation of the PR interval with subsewuent occurence of a single non-conducted P wave = pause.
the pause is shorter than the sum of any 2 consecutive beats |
|
|
what is a Mobitz II second degree AV block?
|
constant PR interval followed by sudden failure of a p wave to be conducted to the ventricles; so an occasional dropped p wave or a regular conduction patter 2:1 , 3:1 etc
|
|
|
what is a high grade AV block?
|
muliple p waves in a row that should conduct but dont. ration must be 3:1 or higher
|
|
|
third degree AV block
|
diagnosed when no supraventricular impulses are conduced to the ventricles. P waves reflect a sinus node rhythm independent from the QRS wave complexes
the QRS represents excape |
|
|
describe the epidemiology of AB block?
|
1st degree foudn in healthy adults, increasesd with age
Mobit II rare in healthy where as Wnechenbach is oberved in 2% of healthy young people congenital 3rd degree in 2% of health people |
|
|
when is wenckebach and congenital 3rd degree AV blockespecially commonly obseved in young people:
|
during sleep
|
|
|
3rd degree AV block is associated with what symptoms?
|
fatigue, dizziness, lightheadedness, presyncope, syncope
|
|
|
what is ventricular tachycardia?
|
>100bpm arising distal to the budle of His
|
|
|
true or false
VT is associated with a risk of sudden death |
true
|
|
|
describe monomorphic VT
|
single focus, identical QRS complex
|
|
|
what are some risk factors for Ventricular tachycardia?
|
electrolyte abnormalities
RFs for IHD or CAD use of sympathomimetic drugs sysemic diseses like SLE, haemochromatosis, RA congenital heart disease digitalis toxicity channelopathies |
|
|
which antiarrhythmic drugs are also a RF for ventricular tachycardia
|
amioderone
dispyramide sotalol |
|
|
Which antipsychotic medications are also a risk factor for ventricular tachycardia
|
amisulpride
droperidol haloperidole sertindole ziprasidone |
|
|
describe a polymorphic ventricular tachycardia
|
Irregular rhythm, caryng QRS morphology/amplitude.
An example is Torsades de pointes |
|
|
differentiate bewteen a sustained and a non-sustained VT
|
sustained is >30sec, thisis a medical emergency and usually assoicated with diminished perfusion
|
|
|
describe the epidemiology of ventricular tachycardia's
|
cause of most sudden deaths
not well defined ~300,000 deaths/year i the US |
|
|
what are the risk factors for a ventricular tachycardia?
|
electrolyte disturbacne
RFs for IHD and CAD use of sympathomimetic drugs Myocardial insult from systemic disease (sarcoidosis SLE, haemochromatosis, RA) congenital heart disease digitalis toxicity channelopathies sleep apnoea drugs that prolong QT interval |
|
|
list some ant-infective agents which may cause a ventricular tachycardia
|
atazanavir
chloroquine clarithromycin erythrimycin fluconazole mefloquine, moxifloxacin pentamidine quinine voriconazole |
|
|
list 4 steps that can cause a pathology leading to a entricular tachycardia
|
1. myocardial scarring frim ischemic heart disease or cardiomyopathy --> fibrotic replacement. --> slows conduction
2. abnormal automaticity of conduction pathways 3. triggered activity --> favours ectopic foci 4. Activation of re-entrant pathways |
|
|
what is a fusion beat?
|
mixed morphology, die to normal AV node/His purkinje conduction occuring simultaneously with abnormal (wide, complex) ventricular depolarization
|
|
|
what is a capture beat?
|
occurs when an atrial impulse arries at the AV node at a 'fortunate' time, when the AV node has just recovered from its refractory period --> normal P wave and QRS complex
|
|
|
if there is a decrease in CO due to rapid HR and uncoordinated atria, what might be the rresponse?
|
diminished myocardial perfusion causes a worsening ionotropic response --> degeneration of VF and sudden death.
|
|
|
how my VT present?
|
syncope, palpitations, SOB +/- haemofynamic compromise
chest pain, anxiety, sensation of neck fullness, hypotension, tachypnoea, low conciouslyness,pallor or diaphoresis. |
|
|
with regards to VT how is adenosine used as a special test?
|
IV infused adenosine used to induce transient AV node block which terminates reentrant SVTs; so SVT will end by the VT will continue.
It was historically used to Ddx b/w regualte wide QRS complex and SVT and VT however it increased to rate of VF |
|
|
what genetic screening might you do in a person with VT?
|
long QT syndrome
arrhythmogenic RV dysplasia |
|
|
in a person with VT, or any arrhythmia, why might a biopsy be performed.
|
to confirm ARVC or infiltrative myopathy.
|
|
|
what is the ongoing treatment for VT?
|
antiarrhythmic drugs in class I, II, III, electrolytes, vasopressors(epinephrine, vasopressin)
pacemaker, ICV, catheter ablation diet |
|
|
in the acute settion how is VT treated?
|
advanced life support protocol + DC current cardioversion with sedation
if cardioversion is unsucsessful adrenaline 2mg IV bolus repeated at 5min intervals until return of spontaneous circulation lidocaine (class IB) 75-100mg IV infusion over 2mins follwed by 4mg/min up to an hour OR amioderone (class III) 5mg/kg IV as bolus then 10-15mg/kg for 24hour |
|
|
what is Torsades de Pointes?
|
polymorphic VT observed in the setting of a prolongued QT interval (prolongued ventricular repolarisaiton). It is frequently self limiting, however it can cause haemodynamic collapse or lead to cardiac arrest
|
|
|
what an cause an acquired prolongued QT?
|
potassium channel-blocking medications such as quinidine, erythromucin, haloperidol
|
|
|
what causes a congenital prolognued QT?
|
genetic disporders involving abnomal cardiac ion channels.
|
|
|
what is the treatment for a torsades de pointes?
|
check the serum K and correct to a goal range or 5-5.5mmol/L
cease any drugs that may be contributing there is dispute about the followin 1. temporary transvenous pacing (90-100bpm) 2. Mgsulfate 50%, 4ml (2g) IV over 10-15mintutes followed by 1.5mL/hour IV infusion up to 24hr 3. Isoprenaline 20mcg followed by slow infusion 4. lignocaine 75-100mg Iv folliwed by slow infusion |
|
|
what is Brugada syndrome?
|
A channelopathy characterised by polymorphic ventricular tachycardia, ventricular filbrillations --> cardiac arrest and sudden death
it is atosomal dominant 50% of cases |
|
|
what mutation is involved in brogada syndrome?
|
10-30% of cases involve mutation in SCN5A gene encoding cardia voltage gated Na channel NaV
|
|
|
where is brugada syndrome more common.
|
asia, particularly thailand
|
|
|
are men or women more affected by brugada syndrome?
|
men; 8:1
|
|
|
what does the ECG typically look like in type 1 ECG of brugada syndrome?
|
type I: ECG pattern with prnounced elevation of the J point, a coved-type ST segment and an inverted T wave in V1 and V2
|
|
|
what does the ECG typically look like in type 2ECG of brugada syndrome?
|
a saddle back ST segment elevated by >1mm
|
|
|
what does the ECG typically look like in type 3 ECG of brugada syndrome?
|
ST segment is elevated by <1mm
|
|
|
which ECG type is diagnostic of brugada syndrome?
|
type 1; pronounced elevatoin at the J point, a coved type ST segment and an inerted T wave in V1 and V2
|
|
|
what is the treatment for brugada syndrome?
|
implantation of ICD
|
|
|
what is wolfe parkinson white syndrome?
|
pre-excitation syndrome. Occurs when one or more strands of myocardial fibres (accessory pathyways) coneects the atrium to the ventriculse across the mitral or tricuspid annula. Conduction will reach this ventrical earlier --> prexcitation; increased risk of arrhythmaia
|
|
|
what is the aetiology of wolfe parkinson white sydnrome?
|
developmental cardical defect in AV insulation at the AV groove due to the present of accessory pathway.
|
|
|
what is the ECG finding of Wolfe parkinson White sydnrome
|
delta wave; slurring of the P and QRS waves and inverted T wave
|
|
|
what is the treatment for wolfe parkinson white syndrome
|
do not treat asymptomatic pts; monitor every 2 years
catheter ablation if episodic AV reciprocating tachycardia. pts can be taught a vagal manouvre or failing that, propranolon 80mg and diltiazem 120mg PRN |
|
|
what is ventricular fibrillation
|
simultaneous presence of multiple actiation wave fronts within the ventricle and no CO
|
|
|
what is the ECG finding in ventricular fibrilltions?
|
there are no true QRS comlets and a chaotic wide tachyarrhythmia
|
|
|
what percental of ardiac deaths result from VF?
|
75%
|
|
|
what perentage of CAD deaths are attributable to VF?
|
~50% (often within first hour of AMI onset)
|
|
|
what are the risk factors for VF?
|
CAD, previous MI, syncope
LV ejection F <35% cardiomyopathy valvular disease myocarditis long QT WPW syndrome brugada syndrome |
|
|
what is the pathology of VF?
|
most commonly ocurs in the clinical situation, and is assoicated commonly with CAD as the terminal event. Scarring --> altered conduction
|
|
|
what are some factrsors that increase the energy required for successful defibrillation:
|
time before defib begins
paddle size paddle-to-myocardium distance (obesity) use of condution fluid (disposable, pads, electrpe paste/jelly) contact pressure elimination of stray conduciton pathways previous shocks, this decreases the defibrilation threshold. |
|
|
what is treatment of VF?
|
most successful remains external electrical defibrillation.
|
|
|
how does extrenal electrical defibrillation work?
|
a shock is deliverd to the hear in order to uniformly and simultaneously depolarize a critical mass of the excitable myocardium.
the objective sare to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of promary pacemaker |
|
|
what are the 2 key factors that contribute to successful defibrilation in a patient?
|
duration beetween the onset of VF and the defibrillation
the metabolic condition of the myocardium. |
|
|
describe the progression of the waveform in a pateint with VF before defibrillation in attempted.
|
the VF wavefront usually begins with a relatively high amplitude and frequency, it then degenerates to smaller and smaller amplitude unti asystole after approxmately 15mintues.
|
|
|
what is the defibrillation success rates for pts in VF?
|
they decreses by 5-10% for each minute after onset.
85% has been reported in monitored settings wher intervention is rapid |
|
|
what is the benefit of using larger paddles in external electrical defibrilation?
|
larger paddles result in lower impedance, this allows the use of lower-energy shocks.
optimal sizes; 8-12.5 for an adult, 4-5-5 for an infant. |
|
|
where do you position the paddles in external electrical defibrilation?
|
one below the outer hald of the righ clavicle and the other over the apex (V4-V5)
|
|
|
what is the primary cause of mitral stenosis?
|
95% is caused by rheumatic heart disease
in the eplderlycan be caused by calcifications |
|
|
describe the pathology of mitral stenosis:
|
in rheumatic disease: the orifice is slowly closed by progressive fibrosis, calcification of leaflets and fusion of the cusps and subvalvular apparatus.
flow from LA to LV is restricted, pressure --> pulmonary venous congestions and dyspnoea. --> LA dilatation and hypertrophy. |
|
|
what is the normal and diseased measurements of the mitral valve?
|
it is mornally 5cm in diastole but can be resuded in mitral stenosis down to <1cm.
symptoms become apparent at <2cm |
|
|
what are some of the complications of mitral stenosis
|
pulmonary HTN -->
RV hypertrophy/dilatation --> tricuspid regurgitation --> Right heart failure |
|
|
what are the sypmtoms/ of mitral stenosis?
|
dyspnoea, orthopnoea, paroxysmal noctural dyspnoea, fatigue, oedema, ascites, palpitatios, haemoptysis, cough, chest pain (pHTN), thromboembolism complications
|
|
|
what are some of the signs of mitral stenosis?
|
AF
mitral facies auscultation; loud 1st HS palapble "tapping apex beat" oepning snap mid-diastolic murmur +/- thrills raised pulmonary pressure --> crepitations, pulmonary oedema, effusions pHTN --> RV heave, loup P2 |
|
|
what will you see on ECG with mitral stenosis?
|
atrial hypertrophy (bifid P waves)
|
|
|
what wil you see on CRX in mitral stenosis?
|
enlarged left atrium, signs of pulmonary venous congestion
|
|
|
what are the classifications of mitral stenosis?
|
mild: gradient <5mmHg, valve area >1.5cm
moderate: gradient is 5-10mmHg and valve area is 1-1.5cm Severe: gradient >10mmHg and valve area <1cm |
|
|
how do you treat minor symptoms of mitral stenosis?
|
medical treatment: antigoabulation, digoxin, beta-blockers, rate limiting CCB, diuretics and antibiotic prophylaxis
|
|
|
what is the definitive treatment of mitral stenosis?
|
balloon valvuloplsasty; indicated when ther are significant symptoms, isolated stenosis with no regurgitaiton and mobile non-calcified valve apparatus on echo
Mitral valvotomy: if the above no available always use AB prophylactics |
|
|
what are some RFs for valve prolapse leading to mitral regurgitation?
|
congeintal disease, degenerative myxomatous changes or connective tissue disorders (Marfan's)
|
|
|
what is the pathophysiology of mitral regurgitation?
|
the Lv slowly dilatates --> LV diastolic and LA pressures gradually increase due to volume overload of LV --> SOB and pulmonary oedema
Acute mitra regurgitation ends to cause a rapid rise in the LA presssure and a marked symptomatic deterioration |
|
|
what are some of the RF for mitral regurgitation
|
valve prolapse
dilatation of LV and the thus the mitral ring (CAD or cardiomyopathy) damage to the valve cusps and chordae (RHD, endocarditis) damage to the papillay muscles post mitral valvotomy or valvuloplasty |
|
|
what are some of the presenting symptoms of mitral regurgitation?
|
dyspnoea, orthopnoea, PND, fatigue palpitations, oedema, ascites, diaphoresis
|
|
|
what are some of the examination findings of mitral regurgitation?
|
AF, Atrial Flutter, cardiomegaly - displaced hyperdynamic apex beat w/ apical pansystolic murmur, soft S1 and S3
signs of pulmonary congenstions |
|
|
in mitral regurgitation what will you see on ECG and CXR?
|
ECG: left/atrial/ventricular hypertrophy
CXR; lateral, enlarged LA/V, pulmonary venous congestion and oedema |
|
|
how is mitral regurgitation graded
|
Asymptomatic:
LVEF>60% and end systolic diameter <45mm - requires medical treatment LVEF <60% and end diastolic diameter >45mm requires surgical treatment Symptomatic LVEF >30% - medical LVEF<30% - surgical |
|
|
what is the definitive treatment ofr mitral regurgitation?
|
valve repair, this is indicated by worsening symptoms and progressie radio cardiac enlargement or echocardiographic evidence of deteriorating LV function
|
|
|
describe the pathology of Aortic Stenosis?
|
CO is initially maintained; this is via increasing the pressure gradient across the aortic alve. LV becomes hypertrophied and coroary blood flow then becomes inadequate --> angina
fixed outflow obstruction limits increases to CO for exertion --> effort related hypotension and syncope LV no longer over come the outflow tract obstruction --> pulmonary oedema. |
|
|
is mild to moderatate aortic stenosis usually symptomatic?
|
no
|
|
|
what kind of murmur do you hear in aortic stenosis?
|
ejection systolic murmur; may radiate to the neck
|
|
|
what are some of the signs found on a cardio examination for Aortic Stenosis?
|
slow rising carotic pulse, narrow pulse pressure, thrusing apex beat (LC pressure overload)
signs of pulm congestion paradoxically spit S2 and a soft S2 |
|
|
what is Gallvardin phenomenon and what valve disease is it associated with?
|
dissociated between the noisy and musical components of a systolic murmur
aortic stenosis |
|
|
what might you find on an ECG in relation th aortic stenosis
|
LV hypertrophy feature
LBBB down sloping ST segment and inverted T |
|
|
what is the treatment for aortic stenosis
|
in asymptomatic pts monitoring 1-2yearl
symptomaticl promp valve replacement required aortic balloon valvuloplasty used in congeital aortic stenosis |
|
|
at what age does aortic stenosis occur?
|
it is a disease of the elderly, however congenital aortic stenosis affects infants and adolescents and calcification and fibrosis of a bicuspid valve affects young adults
rheumatic heart disease also increases the incidence in young people. |
|
|
what are the risk factors for aortic regurgitation>
|
congenital: bicuspid or disproportionate cusps
acquired; rheumatic, infective endocarditis, trauma, aortic dilatation (Marfan's, aneurysm, dissection, syphilis, ankylosing spondylitis, connective tissue disorder) HTN and age |
|
|
what is the pathophys of aortic regurgitation
|
LV dilatates and hypertrophies to conpensate for regurgitation --> stroke output of Lv may double or trebble, --> major arteries become conspicuous and pulatile
as LV diastolic pressure rises --> SOB |
|
|
what murmur us heard in aortic regurgitaion?
|
early diastolic murmur and
Austin flint murmur (soft mid diastolic) may hear a systolic murmur because of high stroke volume) |
|
|
what pulse related signs might you see in aortic regurgitaion?
|
Femoral bruits (Duronziez's sign) and
Head nodding with pulse (de Musset's sign) |
|
|
with aortic regurgitation what might you see on ECG?
|
T wave inversion
|
|
|
in aortic regurgitation how should systolic BP be treated?
|
controlled with nifedipine or ACEi
|
|
|
define a tricuspid stenosis
|
a rare condition. where there is abnormal elevation of the pressure gradient across the tricuspid valve during diastolic filling of the RV
|
|
|
what are the risk factors for tricuspid stenosis?
|
Rheumatic fever
occurs mainly in women does NOT occur as an isolated lesion, usually assoaited with mitral stenosis |
|
|
describe the pathology of tricuspid stenosis?
|
diastolic pressure gradient 4mmHg is enough to elevate the mean RA pressure --> systemic veouns congestions.
this is accompanied by hepatomegaly, ascites, and oedema CO at rest will be depressed, fails to rise in exercise low CO --> normal or slightly elevsted LA. PA and RV systolic pressue despite MS TS can leak masking the haemodynamics and lcinical features of MS |
|
|
what is the symptom profile/presentation of tricuspid stenosis?
|
mitral stenosis usually precedes it so pulmonary congestion and fatigue are the first presentation
|
|
|
what is tricuspid stenosis particularly assoicated with systemically?
|
marked hepatic congestion --> cirrhosis, jaundice, malnutrition, anasarca and ascites.
juglar veins distended, and may be giant waves |
|
|
what murmur is assoicated iwth tricuspid stenosis
|
mid diastolic murmur at lower sternal edge
usually higher pitched than mitral stenosis and increases on inspiration |
|
|
in mitral stenosis, what is seen in ECG
|
RA wave may be very tall, approaching RV systolic pressure.
RA enlargement features - peaked P wavesin lead II and prominent upright P waves in lead V1 |
|
|
what is the treatment plan for tricuspid stenosis?
|
intensive salt restriction, bed rest and diuretic therapy preoperatively
surgery for mitral valvotomy (or balloon valvulopasty) |
|
|
what are the indications for surgical treatment of tricuspid stenosis
|
w/ moderate or severe tricuspid stenosis with a mean diastolic pressure gradient >4mmHg and tricuspid orrifice area <1.5-2cm2
|
|
|
what are some common risk factors for tricuspid regurgitation
|
secondary to dilation of the annulus from RV enlargemnt due to pHTN
rheumatic fever may produce ricuspid regurg with tricuspid stenosis infarction of the RV papillary muscles, prolapse, carcinoid of the heart, endomyocardial fibrosis, radiation, infective endocarditis |
|
|
what are some uncommon risk factors for triuspid regurgitaiton
|
congenital deformity of the valve
ebstein's malformation (tricuspid vave displacement towards the RV apex --> RA enlagement) |
|
|
tricuspid regurgitation leads to what?
|
low CO, elevated RA pressures and atrial distension with reduced contractile reserve (--> AF)
ascites caused by congestion and fibrosis --> chronic liver disease (Cardiac cirrhosis) |
|
|
what are the cardiac signs associated with tricuspid regurgitation?
|
large systolic wave in JVP
may have pan systolic murmur at left sternal edge with systolic pulsation of the liver |
|
|
in tricuspid regurgitation what might you see on ECG
|
inferior Q waves from MI or RVH
|
|
|
describe pulmonary stenosis
|
obstruction of the blood flow from the RV into the pulmonary bed, resulting in a pressure gradient >10mmHg across the pulmonary valve during systole
|
|
|
where is the pathology in pulmonary stenosis?
|
80-90% found at the elvel of the valve but it can also occu below the valve or distally in the pulmonary arteries.
|
|
|
what are the risk factors for pulmonary stenosis?
|
usually congenital
assocaited with tetrology of fallow can occur in carcinoid synrome can be involved in rheumatic heart disease. |
|
|
what is the cause of pulmonary regurgitation
|
caused by dilatation of the pulmonary artery due to pHTN (very rare)
|
|
|
what murmur is associated with pulmoary regurgitation
|
graham steel murmur (high pitched decrecendo diastolic blowing at the left sternal edge)
|
|
|
what triggers acute rheumatic fever?
|
triggered by immune delated response to infection with group A streptococci
|
|
|
how is rheumatic heart disease triggered
|
triggered by immune delated response to infection with group A streptococci
antigens corss react with cardiac myosinand sarcolemmal membrane protein |
|
|
which valve is almost always affected in rheumatic heard disease?
|
the mitral valve - sometimes together with aortic valve.
|
|
|
what is the characteristic manifestiation of rheumatic heart disease
|
mitra regurgitation and/or mitral stenosis sometiems accompanied by aortic regurgitation
|
|
|
describe the pathoogy of rheumatic heart disease
|
characteristic mitral valve involvement; myocardial inflammation amy affect electrical conduction pathway, leading to P-R interval prolongation (first degree AV block rarely higher level) and softening of 1st heart sound.
destructive lytic process of acute rheumatic fever is in chotrast wto chronic whcih is primarily fibrosis. fibrinoud degeneration seen in collagen of connective tissues. Aschoff nodule; pathognomonic |
|
|
what are aschoff nodules
|
pathognomonic of rheumatic heard disease; composed of multinucleated ginat cells surrounded by macrophages and T lymphocytes
|
|
|
what are the cardiac manifestation of rheumatic heart disease
|
pancarditis; invles the endocardium, myoardium and percardium. Incidence declines iwth age (90% at 3y)
can produe SOB (heart failure/pericardial effusion), palpitations, tachycardia, cardiac enlargement |
|
|
what are the arthritic and skin complications of rheumatic fever
|
arthritis: occurs when strep antibody titres are high; acute painful asymmetrical and migratory inflammation of the large jointsl red swollen and tender for 1-2days; respond to aspirin
skin; erythema marginatum; red macules, fade in thecentre and remain red at edge, occur in trunk and proximal extremities; not the face subcutaneous nodules; small firm and painless and are bestfelt over the extensor surface of bone and tendons; occur 3weeks after other symptoms |
|
|
what is a care coombs murmur
|
occurs in rheumatic heart disease; is a soft mid-diastolic murmur due tovalvulitis
|
|
|
what is the treatment for rheumatic heard disease?
|
treating the preceeding infection; penicllin oral
for arthritis aspirin for CCF use prednis(ol)one PLUS bed rest, diuretics and ACEi sydenham's chorea; carbmazepine or Navalproate Mitral valve damage; replacement |
|
|
what is the definition of heart failure
|
heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure.
it results from any cardiac disease that compromises ventricular systolic or diastolic function or both |
|
|
what is the epidemiology of heart failure
|
prevalence is 1-2% in the western world; incidence is 5-10/1000/year
|
|
|
what are some cardiac causes of heart failure
|
CAD (60-70%), cardiomyopathies, HTN(contributes to 75%), myocarditis, valvular disease, congenital heard disease
|
|
|
what are some infective and other caues of heart failure?
|
lyme disease, HIV, infective endocarditis
infiltrative diseases electrolyte imbalance endocrine (DM, thyroid, hypoparathyroidism with hypocalcaemia, phaeochromocytoma, acromegaly) |
|
|
what is the definition of systolic heart failure
|
depressed ejection fraction
pressure overload states (HTN, obstructive valvula diseae) volume overload states (regurg valve disease) chagas disease |
|
|
what is diastolic heart failure?
|
preserved ejection fraction
pathological hypertrophy (HTN and aging) restrictive cardiomyopathy haemochromatosis fibrosis, endomyocardial disorders |
|
|
what is the jones criteria?
|
used in rheumatic heart disease and requires >2 major OR 1 major PLUS >2minor AND evidence of infection
|
|
|
what are the major elements of the Jones Criteria?
|
carditis
polyarthritis chorea erythema marginatum subcutaneous nodules |
|
|
what are the minor criteria of the jones criteria
|
fever, arthralgia, previous RF raised ESR/CRP, leukocytosis, 1st degree AV block PLUS supporting evidence of strep infection e.g., scarlet fever, raised ASO and positive throat swab
|
|
|
what is the definition of diastolic heart failure?
|
preserved ejection fraction
caused by: pathological hypertrophy, restrictive cardiomyopthaies storage disorders haemochromatosis fibrosis, endomyocardial disorder |
|
|
what type of heart failure is haemochromatosis implicated in?
|
diastolic heart failure; preserved ejection fraction
|
|
|
In heart failure, the LV dysfunction may slient. the compensation mechanisms involed include;
|
activation of the renin-angiotensin-aldosterone and adrenergic nervous systems which are responsible for maintaining the CO thourhg increased water and Na retension.
increased myocardial contractility activation of vasodilator molecules ANP, BNP, prostaglandins (PGE2, PG12) and NO that offsetsthe excessive peripheral cascular constriction |
|
|
in heart failure what are the 6 aspects of LV remodelling
|
1) myocyte hypertrphy
2) alterations to contractile properties 3) progressive loss of myocytes thorugh necrosis, apoptosis and autophagic cell death 4)beta-adrenergic desensitization 5) abnormal myocardial energetic and metabolism 6) reorganisation of the extracellular matric that does not provide structural support to the mycotes |
|
|
in heart failure describe systolic dysfunction
|
decreased function of the sarcoplasmic reiculum Ca adenosine triphosphatase resulting in decreased Ca uptake into the SR,
hyperphosphorylation of the ryanodine receptor --> Ca leakage from the SR --> decreased expression of alpha myosin and increased beta myosin, myocytolysis --> impaired ability to contract --> depressed LV systolic fnction |
|
|
In heart failure desceribe diastolic dysfunction
|
myocardial relaxation is ATP dependent.
reduction of ATP i.e., ischemia interfers with process --> slowed myocardial relaxation LV filling pressures is delayed as increased HR that shortens distolic filling and |
|
|
what are some of the respiratory symptoms of heart failure?
|
SOB, paroxysmoal dyspnoea, Cheyne-stokes respiration
|
|
|
what are some of the abdo related syptoms ofheart failure?
|
anorexia, nausea, arly satiety, abdominal pain and dullness (related to GI oedema)
iver congestion and RUQ pain hepatosplenomegaly |
|
|
what are some of the general symptoms of heart failure
|
fatigue, confusion, disorientation and sleep and mood disturbances
|
|
|
describe systolic BP in HF
|
it is reduced in advanced heart failure
|
|
|
what are the cardio signs of heart failure
|
diminshed pulse pressure
sinus tachycardia peripheral cyanosis JVP distended course crackles, wheeze - cardiac asthma displaced apex beat |
|
|
describe some of the biomarkers and there important in heart failure?
|
BNP and NT pro-BNP released from failing heart; sensitive marker for HF with depressed ejection fraction
natriuretic peptive levels, increases with age and renal impairment and in women, must be corrected for this Topnins T and I, CRP, TNF recepors and uric acid may all be elevated |
|
|
describe BNP in heart failure
|
released from the failing heart so is high senstive marker
|
|
|
describe natriuretic peptide in heart failure
|
is increased, but is also increased in renal failure, with age and in women
not as sensitive |
|
|
how is heart failure treated?
|
maintaining good fluid status; adding ACEi and beta blocker if needed
can also add for symptoms improvement aldosterone antagoniist hydralazine/isosorbide digoxin |
|
|
what is Cor pulmonale?
|
alteration in the structure and function of hte RV caused by a primary disorder of the respiratory system
|
|
|
what is the common link between lung dysfunction and cor pulmonale?
|
pulmonary HTN
|
|
|
true or false
right sided ventricular diseasr caused by a primary abonmality in the let side of the heart is also considered or pulmonale |
false
|
|
|
what is te primary pathological aetiology of cor pulmonary
|
pulmonary vasoconstriction due to alveolar hypoxia or blood acidaemia --> pHTN --> Cor pulmonae
|
|
|
what is the most common cause of Cor Pulmonale
|
COPD
|
|
|
what 2 conditions cause acute cor pulmonale?
|
PE and ARDS
|
|
|
describe pulmonary HTN in people at high altitude?
|
pHTN caused by chronic hypoxaemia,
similarly, hypoventilation suffficenct to produce alveolar hypoxia and hypercapniea - occurs in morbidly obese |
|
|
what are some important elements contributing to RV failure in COPD?
|
acidaemia and hypercapnia contribue to RV impairment
|
|
|
describe the remodelling of pulmonary vasculature (with respect to Cor Pulmonale)
|
chronic hypoxaemia and ventilator insufficiency --> vascular remodelling --> medial smooth musclehypertrophy --> distal SM proliferation; neomuscularisation of non-muscular vessels--> increased resisitance -->remodelling --> pressure rises
|
|
|
what shape is the normal RV?
|
cresent
|
|
|
what is the normal wall thickness of the RV?
|
<0.6cm
|
|
|
describe the movements of the RV normally
|
contracts sequenctially, inflow to outflow; passive role in maintaining cardiac output
|
|
|
what is the estimated normal volume of the RV?
|
103ml
|
|
|
when there is an acute increaed in afterlad in the RV what happens?
|
there is a significant fall in the stroke volume - remember this is in contrast to the LV which can accomodate an acute increase in after load with little chanes to the stroke output
|
|
|
In Cor pulmonale the RV must work harder, describe the pathophys of this?
|
there is ventricular myocyte thickening (large nuclei); ventricle will then further hypertrophy to expel a normal stroke output against the pulmonary resistance to maintain CO; crescent shape is lost. now spherical
|
|
|
in cor pulmonale there is a hypertrophy of the RV what does this result in
|
there is increaed Ioxygen consumption, but due to increased thickness there is decreased endocardial perfusion
there is also an incearease in the end diastolic pressure causing RV stiffness = imbalance between RV oxygen demand and supply |
|
|
describe decompensated cor pulmonale?
|
development of RV volume overload with ventricular dilation results in decerased ejection fraction, stroke volume tends to be maintaimed clsoe to normal range in decompendated cor pulmonale.
|
|
|
in cor pulmonale, as the pulmonary pressure continues to rise, what occurs?
|
severe tricuspid regurgitation will compromise the RV output, limiting LV filling --> decreaed LV preload and decreaed CO
|
|
|
what are some of the signs of cor pulmonale
|
left parasternal systolic lift
thud at pulmonary area HS muffled (Due to COPD) pulmonic componene of S2 accentuated and occuts earlier; no splitting just single loud S2 high pitched systolic ejection click sold systolic ejection murmur S3 gallop tricuspid regurg - prominnet blowing pansystolic murmur; increaes with inspiration Graham Steels murmur - soft bowing decrecendo diastolic murmur (in severe PAH) |
|
|
in cor pulmonale what will the ECG show?
|
p wave pattern with rish axis deviation --> increased amplitude in leads II, III and VF >2.5mm
QRS ceor in the frontal plane ofte nshifts to the righ prominent S waves in leads I, II, III reflecting hypertrophy of the cristae supraventricularis |
|
|
what endocrine conditions can cause hypertention?
|
primary aldosteronsism
exogenous steroids NSAIDs Cushing syndrome phaeochromocytoma, congenital adrenal hyperplasia, hypo/hyper thyroidism hyperparathyroidism acromegaly |
|
|
what reno-vascular conditions cause HTN?
|
chronic kidney disease
polycystic kidney urinary tract obstruction renin-rpoducing tumour liddle syndrome |
|
|
what are the systolic classifications/grades of HTN?
|
pre-HTN 120-139
grade 1 140-150 grade 2 160-179 grade 3 >180 isolated systolic >140 w/ <90 diastolic |
|
|
in HTN what are you looking for on fundoscopy?
|
AV nicking, copperwiring, hard exudates, haemorrhage, papilloedema
|
|
|
when measuring BP how slow should the needle be lowered?
|
2-3mmHg/sec
|
|
|
with regards to HTN what is 'non-dipping'?
|
the loss of the usual physiological nocturnal drop in BP - this increaes the cardiovascular risk
|
|
|
what is the aldosterone/renin activity ratio for evidence of promary hyperaldosteronism
|
>20-30
|
|
|
in what is the gold standard for HTN measurement/diagnosis
|
digital subtratction angiography with arterial injection of radiocontrast dye.
|
|
|
what is Idopathic pulmonary artery HTN?
|
a disease of the small pulmonary arteries characterised by cascular proliferation and remodelling.
results in progressive increase in pulmonary vascular resisitance and ultimately --> RV failure --> cor pulmonale. |
|
|
pulmonar HTN is defined as:
|
mean pulmonary artery pressure >25mmHg at rest with pulmonary capillary wedge pressure <15mmHg and pulmonary vascular resisitance >3 woods unites
|
|
|
what are some risk factors for idopathic pulmonary artery HTN?
|
female
FHx Bone morphogenetic protein receptor type 2 mutations stimulants |
|
|
in the new yord hear association/WHO classification of pHTN what is functional class I
|
pt with pHTN with no limitation of usual physical activity, normal activity does not cause symptomes
|
|
|
in the new yord hear association/WHO classification of pHTN what is functional class II
|
mild limitation of physical activty.
no discomfort at rest, but normal phyiscal activity causes increased dyspnoea, fatiague and chest pain |
|
|
in the new yord hear association/WHO classification of pHTN what is functional class III
|
marked limitation of physical activty
|
|
|
in the new yord hear association/WHO classification of pHTN what is functional class IV?
|
pts unable to perform any phyiscial actiity and have signs of RV failure.
|
|
|
in pHTN who are the low risk pts?
|
gradual progressino of disease
no clincal evidence of RVfailure functional class I, II, III 6min walk distance of >400m normal or minimal elevation of BNP minimal RV dysfunction in TTE normal RA pressures |
|
|
in pHTN wou are the high risk pts?
|
rapid progression of disease
evidence of right heart failure functional class IV 6min walk distance <400m pericardial effusion or RV dysfunction of TTE high RA pressure low cardiac index on right heart catheterisation. |
|
|
what are some of the signs present n pHTN
|
peripheral oedema, cyanosis
right sided S3 and S4 early diastolic high pitched murmur in PA palpable left parasterna heave JVP distended |
|
|
what are the treatment options for pHTN/
|
lifestyle modificaiton
vasodilators; CCB (amilodipine, nifedipine) prostacyclin phosphodiesterase type 5 inhibitors? |
|
|
what is Eisenmenger's syndrome?
|
refers to any anomalous circulatory communication that leds to obliterative pulmonary vasculature disease; LT prognosis better in eisenmengers than idopathic pHTN
|
|
|
what is myocarditis?
|
inflammation of the myocardium due to an infection of the myocardium or the effects of circulating toxins, in the absence of the predominant acute or chronic ischemia characterised by CAD
|
|
|
what is the most common infection in myocarditis?
|
Viral and commonly Coxsackie and influenza A/B
|
|
|
which protozoa is often associated with myocarditis
|
tryanamos cruzi (Chagas disease - most common cause of heart failure world wide)
|
|
|
what is the connection of lyme disease and myocarditis?
|
5% will develop myocarditis often associated with degress of AV block
|
|
|
true or false
can cause a dilated cardiomyopathy |
true; in up to 9% of patients
|
|
|
the pathology of myocarditis is charactersited by what?
|
inflammatory cellular infiltrate with or without evidecne of myoyte injury
|
|
|
In the first - viaemic - phase of myocarditis a cardiotropic RNA enters the host myoyte via receptors-mediated endocytosis and then what occurs?
|
Viral RNA is tralsated to the viral protein and the genome is incorporated in the host cell DNA.
This cleaves dystrpophin and is thought to directly cause myocyte dysfunciton |
|
|
the second phase of myocarditis is what?
|
the inflammtory phase
|
|
|
in the inflammatory phase of myocarditis what cells infiltrate and what cytokines do they express
|
Macrophages NK cells and others
IL-1, IL-2, IFNgamma and TNF |
|
|
in myocarditis what is it that causes lysis of myocytes
|
Auto-antibodies directed agaist myocardial contractile and structural proteins are produced which may cause activation of the complement pathway causing myocyte lysis
|
|
|
What is fulminant myocarditis?
|
acute illness following a distinct viral syndrome.
histology shows multiple foci of active myocarditis. |
|
|
what is acute myocarditis
|
Insidious onset of illness and evidence of established ventricular dysfunction. This subgroup may progress to dilated cardiomyopathy.
|
|
|
What is chronic mycarditis
|
insidious onset of illness with clinical and histological relapse with development of LV dysfunction and assoicated chornic recurent inflammatory changes
|
|
|
what is Chronic persistent myocarditis?
|
insidous, with persistent histological infiltrate frequently with foci of mycyte necrosis. no ventricular dysfunction depite other cardiovascular symptoms.
|
|
|
what is infective endocarditis?
|
an infection involving the endocardial surface of the heart, including the valvular structures the chordae tendineae, sites of septal defects or the mural endocardium
|
|
|
what is the most common agent in infective endocarditis?
|
streptococcal viridans
|
|
|
the normal pericardial sac has approximately how much fluid in it?
|
50ml (15-35) to lubricate the surface of the heart
|
|
|
true or false?
congenital absence of the pericardium does not appear to cause clinical or function limitations? |
true
|
|
|
serous pericarditis often producese what?
|
a large effusion of turbid, straw coloured fluid with high protein content.
|
|
|
A haemorrhagic effusion of the pericardium is often due to what
|
malignant disease, particularly carcinoma of the breast, bronchus and lymphoma.
|
|
|
What is cardiac tamponade?
|
acute heat failure due to compression of the heart by a large or rapidly developing effusion.
|
|
|
what is Beck's triad?
|
3 principle features of cardiac tamponade
1. hypotension 2. soft or abent HS 3. jugular venous pressure distension with prominent X decent and absent Y decent. |
|
|
describe an acute pericarditis
|
<6 wks - fibrinous, effusive (serous; sanguineous - containing blood)
|
|
|
describe a sub-acute pericarditis
|
6wks-6months; effusive constrictive (characterised by the combination of tesnse effusion in the pericardial space and constriction by the thichened pericardium) constriction
|
|
|
describe a chronic pericarditis
|
>6months - constrictive effusice and adhesive (non-constrictive)
|
|
|
what is a non-infectious cause of pericarditis
|
MI - usually occurs at 1-3 days later
|
|
|
what is clear indication of pericarditis?
|
the pericardium is well innervated so wil cause severe pain
chest pain is retrosternal and radiates to shoudlers and neck it is aggrevated by deep breathing, movement and change in position |
|
|
describe the innervation of hte pericardium
|
the fibrous pericardium and parietal layer of the serous pericardium are supplied by the phrenic nerve
the visceral layer of the serous pericardium is innervateed by the branches of the sympathetic trunk and vagus nerve. |
|
|
What is a classic sign of pericarditis?
|
a pericardial friction rub; high pitched superficial sratching audible on 85% of pts with percarditis
|
