Cardiovascular Flashcards
what are the conduction velocities of cardiac tissues?
(relative to each other, not absolute)
FAST - purkinje fibres > atrial muscle > ventricular muscle > AV node - SLOW
kawasaki disease Rx
aspirin and IVIG
what is the mechanism and antedote of TCA toxicity?
binds to and blocks inward Na+ channels
also antimuscarinic, alpha-adrenoceptor and histamine receptors
Rx = sodium bicarb, more Na+ for competitive inhibition and alkalinisation of serum ionizes the TCA, stopping its binding to the target channel
by 4 weeks gestation, what has been established in the primitive heart?
beating of the primative heart tube
L/R polarity
2 causes of pulsus paradoxus
- pericardial disease (effusion or constrictive pericarditis) 2. COPD/asthma
what is the distinguishing sign of digoxin toxicity?
yellow vision
ST elevation in V5-6
anteriolateral, distal LAD or LCx
kawasaki disease major complication
coronary artery aneurysm and rupture thrombosis and MI
what branch of the coronary circulation supplies the inferior surface of the heart?
what part of the heart is the inferior surface?
posterior descending/interventricular artery
2/3 is post wall of left ventricle, 1/3 is post. wall of right ventricle
how does flow mediated dilatation occur?
increased flow, increases shear stress on endothelium
opens shear-activated K+ channels, hyperpolarisation
K+-gates Ca++ channels open, Ca++ increases within the cell
Ca++-dependent activation of eNOS, NO generation
vasodilatation
what are the class IB antiarrythmics?
Lidocaine and mexiletine
function of ductus arteriosus
shunts blood from the pulmonary trunk to the descending aorta due to high pulmonary arterial resistance
mixing of very oxygenated with very deoxygenated blood gives PaO2 of 30 mmHg to foetus which is adequate
harsh systolic crescendo-decrescendo murmur heard best at the lower left sternal border
HOCM
WG blood finding
positive cANCA - levels correlate with disease activity
what is the mechanism and adverse effect of nitroprusside?
short acting direct NO release causing increased cGMP
cyanide toxicity
what channel does dihydropyridine calcium blockers target?
L-type voltage gated Ca++ channels
apart from holosystolic MR murmur, which is the best aucultatory finding indicating severity of disease?
S3 gallop - reflects degree of left ventricular volume overload.
How long can myocardial ischaemia continue before damage is irreversible?
30 mins
following MI, what histological changes are apparent between 1 - 5 days? (2)
contraction band necrosis neutrophil infiltrate
what percentage of medium size artery must be stenosed to yield end-organ complication?
70%
tuncus arteriosus gives rise to
ascending aorta and pulmonary trunk
2 most common causes of aortic dissection
- HTN (older)
- connective tissue disorder (Marfan & ED, younger)
only organ spared by polyarteritis nodosa
lung
which drugs help close and maintain ductus arteriosus?
close - indomethacin
maintian - PGE1 and PGE2
3 complicaton of thoracic aneurysm
- aortic regurgitation 2. thrombosis/embolism 3. compression of mediastinal structures
define type B aortic dissection
aortic dissection exclusively involving the thoracic aorta
equation for EF
LVEF becomes symptomatic at?
(EDV-ESV)/EDV
‘what has been ejected’/’what was in there to begin with’
around 40% LVEF begin to experience symptoms
what is the reaction catalysed by eNOS?
Arginine + O2 –> NO + citrulline
increased cytosolic Ca++ activates eNOS; NO activates guanylyl cyclase to make cGMP
What process produces an S3 heart sound?
S3 occurs early in diastole as blood flows against a stiffened left ventricle
clinical features of HOCM (3)
- decreased CO (LV cannot fill in diastole) 2. sudden death due to ventricular arrhythmia (young athlete, sudden death) 3. syncope with exercise
mutation in what protein gives rise to hypertrophic cardiomyopathy? mode of inheritance?
sarcomere autosomal dominant
TCA Rx
as soon as confirmed elevated ESR start IV corticosteroids to prevent blindness
what cell types provides the major proliferative stimulus for cellular component of atheroma?
what does this activate?
platelets - PDGF and TGF-beta
SMC migration from media to intima and proliferation, interstitial collagen production
blood in umbilical vein has PO2 of?
30 mmHg
what is the electrocardial adverse effect of type IA antiarrythmics?
prolonged QT, torsades de points
in traumatic deceleration injury, what part of the aorta is likely to dissect/rupture?
aortic isthimus, where the aorta is held stationary by the ligamentus arteriosus
just after the left sebclavian artery leaves at the top of the descending aorta
in which portion of the developing heart is a VSD most likely to occur?
membranous intraventricular septum
hyaline arterioloscelrosis - aetiology (2)
benign HTN diabetes (non-enzymatic glycosylation)
what are the class IA antiarrythmics?
quinidine, procainamide, disopyramide
following MI, what histological changes are apparent between 4 - 12 hours? (4)
early coagulation necrosis oedema haemorrhage wavy fibers
congenital RFs for cerebral aneurysm (4)
- coarctation of aorta 2. PCKD 3. connective tissue disorder (Elhers-Danlos) 4. AV malformation
what is supplied by LCX?
lateral and posterior walls of left ventricle
papillary muscle
primitive ventricle gives rise to
trabeculated part of left and right ventricles
kawasaki disease main vessel involvement
coronary artery
what is a co-dominant circulation?
posterior descending/interventricular artery arrises from both the RCA and the LCX
7%
how does hydralazine work?
increase cGMP leading to smooth muscle relaxation
preferential vasodilatory action on arterioles > veins, reduces afterload
Brugada syndrome
- inheritance
- EKG findings
- protein affected
- major complication
- Rx
- AD
- psuedo-RBBB & ST segment elevation in V1-3.
- myocardial sodium channelopathy
- sudden cardiac death from ventricular tachyarrhythmia
- implantable cardiac defib
Acute Rheumatic fever symptoms JONES
J - joint arthritis O - ‘heart’ = pancarditis N - nodules E - erythema marginatum S - Sydenham’s chorea
most common causative organism for bacterial endocarditis
strep viridans
TCA epidemiology
old adults (>50 y/o) females
complications of aortic stenosis (3)
- concentric left ventricular hypertrophy 2. angina and syncope with exercise 3. haemolytic anaemia (schistocytes)
in lung histology, haemosiderin laden macrophages reflect what underlying process?
left heart failure increase pulmonary capillary pressure compromise of blood-gas barrier and extravasation of erythrocytes phagocytosis by resident alverolar macrophages and conversion to haemosiderin
is anteriolateral or posteriomedial papillary muscle rupture more likely? why?
posteriomedial - receives only blood from the posterior descending/interventricular artery
anteriolateral papillary muscles have dual blood supply from LAD and LCx
how can you best heard S3 and why?
at end expiration in the left lateral decubitus position
reduces lung volume and brings the left heart closest to the chest wall. Also increases pulmonary venous return to heart by closing small vessels in the lung
which ion channel is only responsible for the rate of action potential firing from pacemaker cells?
i.e. no inotropic or lusitropic effect
what drug can be used to target this?
funny sodium channels
more open - slower refractory period, more closed - longer refractory period
refractory period ==> length of diastole
ivabradine
what are the steps in the pathogenesis of infective endocarditis? (4)
- disruption of normal endocardial surface
- fibrin deposition and nidus formation
- microoganisms colonise the nidus, further coagulation
- macroscopic vegiation formation from RBCs, neutrophils, platelets and microorganisms
ST elevation in V3-4
distal LAD
what are the side effects of amiodarone?
pulmonary fibrosis
blue/grey skin deposits
hepatotoxicity
hypo-/hyper-thyroidism (amIODarone)
in Tet of Falot, what is the factor determining symptom severity?
degree of pulmonary artery outflow obstruction
TCA is associated with another condition?
polymyalgia rheumatica - proximal myalgia and weakness
difference between acute and sub acute bacterial endocarditis?
acute - staph aureus, large vegitations that destroy the valve subacute - smaller vegitations that do not destroy the valve
Ortner syndrome
mitral stenosis causing dilation of the left atrium and subsequent impingement on the left recurrent laryngeal nerve, resulting in hoarsness
hyaline arterioloscelrosis - complication
glomerular scarring –> CKD shrunken kidney
what structure of the primitive heart is defective in Tet of Fallot?
infundibular septum, part of conal septum
due to failure of migration of neural crest cells
4 complication of atherosclerosis
- stenosis 2. thrombosis 3. embolism 4. aneurysm
layers of arterial wall inside to out - major component of each
intima - endothelium media - smooth muscle adventitia - connective tissue
CK-MB is useful in what setting? why?
reinfarction Troponin I remains elevated after first MI, whereas CK-MB is cleared within 72 hours (versus 7 - 10 days)
what is the coronary steal phenomenon? what drugs cause it?
paradoxically, in MI coronary vasodilators divert blood to the low resistance vessels, reducing collateral arteriolar flow to the myocardium distal to any blockage.
dipyridamole, adenosine
3 groups of patients that get Kaposi sarcoma
- older, eastern European male - tumour localised to skin 2. transplant patient 3. AIDS
what is milrinione and when is it used?
PDE3 inhibitor allowing cAMP accumulation in tissues
vasculature = vasodilation
heart = positive inotropy and chronotropy
use in decompensated HF short-term
pathology - HTN causing aortic dissection
vasa vasorum deliver oxygen to media/adventitia of large veseel HTN induces hyaline arteriolosclerosis in VV VV become stenotic weakening of aorta SM wall
which organisms cause endocarditis with negative blood cultures? (5)
HACEK haemophilus actinobacillus cardiobacterium Eikenella Kingella
immediate management of TOGA in newborn?
identify the other malformation that allows mixing of blood and maintain it
TOGA is incompatible with life without PFO, PDA etc.
postnatal derivatives:
ductus arteriosus
ligamentum arteriosum
what are the pressures of the heart?
RA, RV, PA, LA, LV, root of aorta
RA <5
RV 25/5
PA 25/10
LA <10
LV 120/10
aortic root 120/80
when is Mg++ useful as an antiarrhythmic?
torsades de points and digoxin toxicity
Tet of Fallot typical ausculatation findings?
harsh, systolic ejection murmur over mid-to-left sternal border
RVOT obstruction
5 causes of restrictive cardiomyopathy
- amyloidosis 2. sarcoidosis 3. haemochromatosis 4. endocardial fibroelastosis 5. Loeffler syndrome
inspiratory splitting of S2
patent ductus arteriosus
complication of MI in 1st day (3)
- cardiogenic shock 2. congestive heart failure 3. arrhythmia (most common)
major mechanism of GTN
VENOUS dilatation, decrease preload to heart, decrease oxygen requirement
what vessels do the fourth aortic arch contribute to?
true aortic arch and subclavian arteries
complication of MI in 1st month (3)
aneurysm, mural thrombus, Dressler syndrome (AI pericarditis 6-8 week following infarction)
primitive atrium gives rise to
trabeculated part of left and right atria
what does phentolamine do?
non-specific alpha 1/2 blocker with no beta blocker effect
what Ca channel blocker do you use in hypertensive emergeny?
nicardipine, clevidipine
primitive pulmonary vein gives rise to
smooth part of left atrium
Churg-Strauss histopath
necrotizing granuloma (c/o microsocpic polyangiitis) eosinophils (assoc Asthma)
following MI, what histological changes are apparent between 12 - 24 hours? (2)
coagulation necrosis contraction band necrosis
describe the process of septation of the atria in 7 steps
- septum primum, foramen primum
- foramen secundum
- septrum secundum
- foramen ovale
- septum primum expands
- fusion of septa secundum (rostral) and primum (caudal)
- closure of FO with increasing LA pressure at birth
what antiarrythmic drug gives luminous phenomena/visual brightness as adverse effect?
ivabridine
major risk factor for Buerger disease
smoking
in the setting of AF, where in the heart are clots likely to form?
left atrial appendage
what is Ebstein’s anomaly?
downward displacement of the tricuspid valve allowing regurgitant flow from RV to RA and right heart failure
aetiology of S3 (3)
- athletic left atrium pushing blood against healthy left ventricle 2. low ventricular compliance 3. high end-diastolic LV volume (overfilled)
what are the two vessels that can supply the SAN?
right coronary (60%)
left circumflex (40%)
ARF - histo features of myocarditis (4)
Ashoff bodies - foci of chronic inflammation - containing: Anitschkow cells - histiocytes with long, slender nuclei (caterpillar)
Giant cells
fibrinoid material
blowing, loud, holosystolic murmur at left mid sternal border
small VSD audible at days 4 - 10 of life
what is the effect of adenosine on the heart?
prolongs phase 4 of cardiac action potential by activating A1 receptor, reducing the rate of action potentials and lengthening diastole
A1 receptor activates outward K+ channels and blocks inward Ca++ channels
slows sinus rate and increases AV nodal conduction delay - used in pSVT to terminate tachyarrhythmia
borders of the femoral triangle
superior - inguinal ligament
lateral - sartorius
medial - adductor longus
where does the thoracic duct entre the thorax?
through diaphragm at T12 through aortic hiatus
what is the mechanism of ivabridine?
when do you use it?
slows funny Na+ current, negative chronotropy without inotropic effect
reduces cardiac O2 consumption
chronic stable angina in people who do not tolerate beta-blockers
ST depression in V1-3 with tall R waves
posterior, so opposite changes to electrical activity in anterior leads
posterior descending/interventrical artery
blood supply to the retina starting from the common carotid..
common carotid, internal carotid, opthalmic, retnal (within the optic nerve)
how do you treat hypertension in pregnancy? (not pre-eclampsia)
hydralazine, methyldopa, labetolol, nifedipine
micoscopis polyangiitis blood finding
pANCA