Cardio Week 5 Flashcards
what causes the decrease of blood flow in acute coronary syndromes
rupture of atherosclerotic plaque resulting in thrombus
what markers does myocardial damage release
troponin T and I (also enzyme CK)
what is the diagnosis of NSTEMI
elevated levels of these markers but no ST elevation
what is the diagnosis of unstable angina
demonstrate symptoms of ACS but have neither ST elevation or raised troponin
what may NSTEMIs and UA be associated with in terms of an ECG
ST depression and T wave inversion
what are the symptoms of UA/NSTEMI
resemble those of stable angina, but are frequently more painful, intense and persistent, often lasting at least 30 minutes
what is the typical presentation of UA/NSTEMI
unrelieved by GTN, angina of recent onset brought on by minimal exertion, angina at rest/minimal exertion or post MI angina
what is the physiopathology of UA/NSTEMI
compared to stable, plaques found in ACS tend to have thinner fibrous cap and larger lipid core - especially vulnerable to being ruptured
this exposed plaque (vulnerability to rupture) causes what
platelet aggregation and thrombosis causes local generation of vasoconstrictors such as thromboxane A2 and seratonin
when is revascularisation considered for patients in UA/NSTEMI
patients with high risk of very significant coronary arerty disease, or if drug treatment fails to control symptoms
what drugs are immediately given in UA/NSTEMI
300mg aspirin (antiplatelet) then 75mg/day for life also clopidogrel which inhibits ADP stimulated platelet aggregation
what drugs could be given in the long term after UA/NSTEMI
LMWH (antithrombin - daltparin), glycoprotein IIb/IIa (antiplatelet - tirofiban - given after PCI) B blockers, nitrates (temporary basis to relieve pain)
how is a coronary artery bypass grafting performed
left internal thoracic (mammary) artery used rather than saphenous vein LITA not disconnected from parent (subclavian) but cut distally and attached to coronary artery Usually performed on bypass
what are the main complications of coronary artery bypass grafting
systemic inflammatory response, atrial fibrillation and persistent neurological abnormalities
what is the steps of percutaneous coronary intervention
guiding catheter introduced via femoral, brachial or radial arteryguided wire then advanced down lumen of coronary artery until it is positioned across stenosisballoon catheter advanced over this wire and inflated at side of stenosis to increase luminal diameter
what was introduced as part of PCI to prevent elastic recoil and restenosis
stent - cylindrical metal mesh or slotted tubes that are implanted into artery at site of balloon expansion
what is a complication of PCI
thrombosis (controlled by aspirin and clopidogrel)
when is a patient preferred to have revascularisation
when at risk of developing worsening ischaemic disease or whom drugs are not controlling symptoms
when is PCI preferred
when one or two arteries diseased, as long as disease is not too diffuse
when is CABG used
when all three main coronary arteries diseased, when left coronary mainstem has significant stenosis, when lesions not amendable to PCI and when LV function poor
in which of PCI and CABG must revascularisation be repeated more often
PCIimprovements in stenting will narrow this difference
ruptured plaque reveals collagen which serves as site of platelet adhesion, activation and aggregation. This results in what
release of TXA2, fibrinogen, 5HT, platelet activating factor and ADP which further promotes platelet aggregation activation of clotting cascade leading to fibrin formation and propagation and stabilisation of occlusive thrombus
what is hypokinesis
immediate loss of contractility in affected myocardium
what is symptoms of MI
crushing chest pain, radiated into arms, neck, jawsweating, anxiety, clammy skinoften little effect on BP and HR
what is the immediate treatment of a STEMI
Morphine, Oxygen, Nitrates, Aspirin + Clopidogrel Also thrombolytics
what is the long term treatment of STEMI
B blocker, aspirin, ACE inhibitor, reduction of risk factors, revascularisation if high risk of further events
what is thrombolysis
dissolution of blood clot - done in community by ambulance if they cant get to hospital in 120 minutes
how does thrombolysis work
they induce fibrinolysis, fragmentation of fibrin strands holding clot together - permits reperfusion of ischaemic zone
what are the main agents used in thrombolysis
streptokinase (SK) and tissue plasminogen activator (tPA)
what are the risks in thrombolysis
bleeding, intracranial haemorrhage
what are the contradictions in thrombolysis
recent haemorrhagic stroke, recent surgery or trauma and severe hypertension
death is an obvious complication of STEMI. What is the arrhythmic complications
ventricular tachycadia
what is the structural complications of STEMI
cardiac rupture, ventricular septal defect, mitral regurgitation, acute pericarditis
what is Dresslers syndrome
structural complication - pericarditis many weeks post MI, damages heart muscle release previously un-encountered material that stimulates an immune response
what are functional complications of STEMI
ventricular dysfunction (L, R or both), chronic HF, cardiogenic shock
what is the secondary prevention measures of MI
healthy lifestyle, smoking cessation, good control of BP cholesterol and diabetes
what are the four phases of cardiac rehabilitation
in patient, early post discharge period, structured exercise programme (hospital based), long term maintenance of physical activity and life style change
what are the targets of MI rehabilitation and secondary prevention
avoid smoking, healthy diet, regular aerobic exercise, optimal drug therapy, cholesterol <4.0mmol/l BP<140/85mmHg
what is the role of interstitial fluid
acts as the go between blood and body cells
terminal arterioles regulate regional blood flow to capillary bed in most tissues - what regulates flow in a few (eg mesentery)
precapillary sphincters
what substances cannot cross capillary wall
plasma proteins
what is the movement of lipid soluble substances
go through endothelial cells of capillary
what is the movement of water soluble substances
go through water filled pores
how are exchangeable proteins moved across wall
by vesicular transport
what is net filtration pressure proportional to
forces favouring filtration - forces opposing filtration
what are the starling forces which favour filtration
PC - capillary hydrostatic pressure (most important) - 35mmHg at arteriolar, 17mmHg at venule πi - interstitial fluid osmotic pressure - 1mmHg (arteriolar)
what are the starling forced opposing filtration
π c - capillary osmotic pressure - 25mmHgPi - interstitial fluid hydrostatic pressure - 1mmHg
how to calculate net filtration pressure
(PC + πi) - (πc + Pi)
what is NFP at arteriolar end
+10mmHg
what is NFP at venular end
-8mmHg
what do starling forces favour
filtration at arteriolar end, reabsorption at venular end
what is oedema
accumulation of fluid in interstitial fluid
what causes the raised capillary cause of oedema
arteriolar dilation raised venous pressure - left ventricular failure (pulmonary oedema), RVF (peripheral oedema - pitting oedema in ankles or sacram)or prolonged standing
what is the plasma osmotic pressure in oedema and what causes this reduction
<30g/l by malnutrition, protein malabsorption, excessive renal excretion of protein and hepatic failure