Match the artery to the supply of myocardium and leads of ECG
....R) Atrium, SA & AV nodes, Inferior wall of R) ventricle....Lead 1,2 & AVF
...Inferior wall of R) Ventricle, Apex of Heart....Leads 1, 2 & AVF
R) Posterior Interventricular....R) & L) ventricles, Posterior intermuscular septum....Leads (depression)
....L) ventricle anterior wall, Anteroseptal, Anteroapical....V1-4,
....Left Atrium, Left Ventricle, Anterolateral Wall...V5-V6, Lead 1, avL
Macrophages which are transformed into foam cells, secrete cytokines which propagate atherosclerosis?
ST segment: The ST segment represents the time interval at the end of ventricular depolarisation
Ventricular contraction( ventricular depolarisation, Ventricular contraction ) to the time of ventricular repolarisation
ventricular contraction( ventricular repolarisation, ventricular contraction ). At this time there is no difference in electrical potential, therefore there is no deflection, and this segment should be isoelectric.
Changes in the ST segment are caused by disturbances in repolarisation and may be reflected in elevation or depression of ST segment.
The ST segment is measured from the end
start( end, start ) of the QRS complex to the beginning
end( beginning, end ) of the T wave.
Which of these are characteristics of PR interval?
Measured from end of P wave to beginning of QRS?
Measured from start of P wave to beginning of QRS?
Represent time required for impulse to depolarise atria, traverse AV node and enter ventricular system.
QRS complex: Normal duration/ interval 0.08- 0.10
0.12-0.20( 0.08- 0.10, 0.12-0.20 ) secs. The QRS complex reflects ventricular
atrial( ventricular, atrial ) depolarisation (NOT ventricular contraction, which is associated with ST). Not every QRS complex contains a Q wave, R wave and S wave; it depends on the position of the lead and underlying myocardium.
Angina is caused by decreased blood supply within the coronary arteries causing . It normally occurs during periods of strenuous activity where the heart cannot meet the O2 requirements of the myocardial tissue.
Stable angina- physical exertion, to rest and medication
Unstable angina- does not respond to rest or medication
Variant angina- Caused by spasm
Treatment of angina is normally through?
GTN- causes vasodilation of the coronary vessels via increased cGMP
Aspirin- irreversibly inhibits COX enzymes which reduces prostaglandins and thromboxane
The pathology of coronary artery atherosclerosis involves chronic
acute( chronic, acute ) endothelial injury, endothelial dysfunction, smooth muscle migration from tunica media
tunica externa( tunica media, tunica externa ) to tunica intima, engulfment by macrophages
lipids( macrophages, debris, lipids ), formation of foam cells, proliferation of SMC's and collagen.
Which layers will typically be first to undergo infarction?
List the most common pathological conditions affecting the pericardium?
Cardiac Tamponade- fluid within the pericardial sac
Pericarditis- inflammation of the pericardium relieved by sitting up and worsened by supine
Pericardial effusion which can be haemoserous, fibrinoserous, suppuratives.
GTN is A prodrug
vasopressor( prodrug, vasopressor ) which first must be denitrated to produce its active form nitrous oxide
nitrous oxide synthase( nitrous oxide, nitrous oxide synthase ). Nitrous oxide released increases guanylyl cyclase
adenylyl cyclase( guanylyl cyclase, adenylyl cyclase ) activity this results in increased cyclic GMP dependent protein kinase that activates MLC phosphatase
kinase( phosphatase, kinase ). MLC dephosphorylation
phoshorylation( dephosphorylation, phoshorylation )-- VSMC relaxation.
B- blockers competitively antagonise B-adrenergic receptors in cardiac nodal tissue and myocytes. They block NA & A from binding. B-adrenergic receptors are couped to a G-Protein, which activates adenylyl cyclase to form cAMP from ATP. Increased cAMP activates a cAMP dependent protein kinase A that phosphorylates L-type calcium channels, which causes increased calcium entry into the cell. Contraindications to b-blockers are?
Aspirin irreversibly inhibits COX enzyme. Which line of cyclo-oxygenase will regenerate first?
Which factors does heparin inhibit in order to prevent the coagulation cascade form forming fibrin.
Warfarin inhibits activation of vitamin K via inhibition of vitamin k epoxide.
Dual therapy of and aspirin is used because the endothelial cells will eventually replenish the levels of prostaglandin and thromboxane, but can inactive platelets for a lengthy period of time until they are replenished by haemopoeisis.