Ischaemic Heart Disease and Hypoxia Flashcards
what is ischaemic heart disease?
the term given to heart problems caused by narrowed heart (coronary) arteries that supply blood to the heart muscle.( Mismatch between demand and supply)
IHD manifests clinically as?
MI
ischaemic cardiomyopathy
Signs and symptoms of IHD
chest pain/angina
heart rhythm problems
general symptoms
chest pain in IHD
Aching, burning, fullness, heaviness, numbness, pressure, squeezing
Radiation in arms, back, jaw, neck, shoulder
High or low BP
Syncope
heart rhythm problems of IHD
Palpitations
Heart murmurs
Tachycardia
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation
S4gallop: early finding of diastolic dysfunction
S3gallop: indication of reduced left ventricular function and a poor prognostic sign
general IHD symptoms
Nausea, sweating, fatigue or shortness of breath, weakness or dizziness
Reduced exertional capacity
Leg swelling (when left ventricular dysfunction is present)
Diaphoresis
highest prevalence of IHD by age
80-89
highest incidence of IHD by age
85-95+
IHD is a very high common cause of death where geographically?
eastern europe, north africa, india, russia
over __% of CVD is caused by modifiable risk factors
70
non-modifiable risk factors of IHD
age gender family history ethnicity genetics previous history of CVD
modifiable risk factors of IHD
high BP cholesterol stress smoking diabetes BMI low socioeconomic status diet exercise alcohol
Highest risk risk factor
dietary risk
Coronary blood flow to a region may be reduces due to OBSTRUCTION caused by?
Atheroma Thrombosis Spasm Embolus Coronary ostial stenosis Coronary arteritis
A general decrease of oxygenated blood flow to myocardium due to?
anaemia
Carboxyhaemoglobulinaemia
Hypotension causing decreased coronary perfusion pressure
Fibrous fatty lesions are ____ likely to regress than fatty streaks.
less
Fibrous cap of an atherosclerotic plaque is composed of?
layers of smooth muscle cells ensconced in a substantial extracellular matrix network
Fibrous cap as an effective barrier prevents?
plaque rupture
The production of what maintain fibrous cap quality?
TGF-β by T-reg cells and macrophages
By what mechanism is the fibrous cap maintained?
potent stimulation of collagen production in VSMC
How does a vulnerable plaque rupture?
increased + unresolved inflammatory status > thinning of the fibrous cap > prone to rupture exposing prothrombotic components to platelets and pro-coagulation factors > thrombus formation
presentation of coronary/ischaemic heart disease
asymptomatic chronic stable angina unstable angina NSTEMI STEMI heart failure sudden death
coronary embolus
blood clot can break away and block a more distal artery
thrombus formation
atherosclerotic plaque breaks up > direct contact with flowing blood > platelets adhere to it, fibrin deposited, RBC trapped to form clot
blood clots in coronary arteries can grow to cause?
acute coronary occlusion
collaterals in an acute episode
dilate within seconds, doubling by every 2nd or 3rd day usually reaching normal coronary flow in 1 month
what are coronary collaterals?
“natural bypasses,” anastomotic connections w/o an intervening capillary bed between portions of the same coronary artery and between different coronary arteries
collaterals in chronic atherosclerotic patients
Slow occlusion-collateral vessels can develop at the same time while the atherosclerosis becomes more and more severe.
with the presence of collaterals, why do patients still get issue?
collaterals can also get atherosclerosis or damage is so extensive that even collaterals can’t help > can cause weakening of the heart > HF
after acute occlusion > ischaemia > ?
infarction
pathogenesis of myocardial infarction (soon after)
Small amount of collaterals open + blood seep into the infarcted area > local blood vessels dilate and area becomes overfilled with stagnant blood > muscle uses all O2, Hb > deoxy & blood vessels appear engorged despite lack of blood flow
pathogenesis of myocardial infarction (later stages)
Vessels walls permeability increases, fluid leak and local tissue oedematous
Cardiac muscle cells swell and due to no blood supply die within few hours
causes of death following a myocardial infarction
decreased cardiac output - systolic stretch and cardiac shock, damming of blood in venous system, ventricle fibrillation, rupture of infarcted area
effects of small area of ischaemia
little or no death of muscle. Might become non functional temporarily due to lack of nutrients
effects of large area of ischaemia
Some in the centre die rapidly within 1 to 3 hours due to complete loss of blood supply
Immediately around is non functional area failure of contraction and impulse conduction
Surrounding non-functional still contracting but weak due to mild ischemia
risk assessment tools for cardiovascular
JBS3
QRISK
clinical history for IHD
symptoms: chest pain type, associated symptoms and signs, age, sex, ethnicity, smoking, FH
clinical examination for IHD
heart auscultation
BP
BMI
GPE
lab tests for IHD (lipid profile)
LDL HDL triglycerides lipoprotein A C reactive proteins
Serum markers in patients with suspected acute cardiac events (ACS, MI)
Troponins(I or T)
Creatine kinasewith MB isozymes
Lactate dehydrogenase and lactate dehydrogenase isozymes
Serumaspartate aminotransferase
Biomarkers for predicting death were the following:
B-type natriuretic peptide CRP Homocysteine Renin Urinary albumin-to-creatinine ratio
what would you see on ECG with stable angina?
Pretty much normal ECG if you want to see the changes do an exercise stress test
During stress test might see ST depressions indicating IHD
what would you see on ECG with unstable angina/NSTEMI?
ST depression and T wave inversion
what would you see on ECG with acute MI/STEMI?
ST elevation with T wave inversion
Q waves
transthoracic echocardiography helps to assess?
left ventricular function
wall-motion abnormalities in the setting of ACS or AMI
mechanical complications of AMI
transoesophageal echocardiography is used for assessing?
possible aortic dissection in the setting of AMI
stress echocardiography can be used to assess?
evaluate hemodynamically significant stenoses in stable patients who are thought to have CAD
coronary angiography procedure
iodinated contrast agent injected through catheter placed at ostium of coronaries > contrast visualized through radiographic fluoroscopic heart examination
coronary angiography is gold standard for?
detecting stenoses that may be revascularized through percutaneous or surgical intervention
ultrasonography
the common and internal carotid arteries is a noninvasive measure of arterial wall in asymptomatic individuals > combined thickness of the intima + media associated w/ prevalence of cardiovascular risk factors and ^ risk of MI + stroke
doppler velocity probes
for measuring coronary flow in humans
pharmacological treatment for IHD
HMG-CoA reductase inhibitors Bile Acid sequestrants calcium channel blockers ACE inhibitors betablockers anti-anginal agents platelet aggregate inhibitors nitrates
revascularisation therapies
percutaneous coronary intervention (angiohgraphy + stent)
CABG (vessel from somewhere else used to make a graft)
WHO recommendations for prevention
physical activity avoid smoking balanced healthy diet maintain a normal body weight reduce stress
