chest pain Flashcards
Ischemic heart disease
imbalance between supply and demand for oxygen and nutrients and removal of metabolites
Hypoxemia vs Ischemia
Mild disease- ATP pump failure ion leakage (K+), lack of collateral blood flow= metabolite build up (lactate), reversible (angina)
Severe or prolonged disease- membrane damage (enzyme released), cell death and tissue necrosis (cardiac biomarkers), Irreversible (infarction)
Ischemic heart disease- epidemiology
leading cause of death and disability in USA
Death rate decreased since 1963- Preventative measures- directed against development of atherosclerosis (Smoking, cholesterol, HTN, lifestyle)
Therapeutic advanced- medical and surgical
Only 20% of pt with chest pain have ACR
IHD pathogenensis
diminished coronary blood flow relative to myocardial demand–> Ischemia
cause of IHD- reduced coronary blood flow due to atherosclerotic narrowing (>90%)
Other causes- lowered systolic blood pressure, vasculitis, structural anomaly, severe HTN, diminished oxygenation or diminished oxygen carrying capacity
Fixed obstruction
Anatmic narrowing/occlusion- narrowing o f >70% causes symptomatic ischemia with exercise
> 90% stenosis causes ischemia at rest
Often multiple arteries are affected- most commonly (first several cm of left anterior descending (LAD), left circumfles, entire length of right coronary artery (RCA)
Effects modified by collaterals
acute plaque change
unpredictable, abrupt confversion of stable plaque to an unstable atherothrombotic lesion that results in myocardial ischemia
Rupture/fissures/ulcerations- exposes underlying thrombogenic substances
Hemorrhage into atheroma- expands plaque and further narrows lumen
Results in acute coronary syndromes- acute MI, unstable Angina, sudden cardiac death
influences contributing to acute plaque change
intrinsic factors- structure and composition of plaque- large areas of foam cells and lipid, thin fibrous cap, most dangerous lesions are the moderately stenotic (50-75%) lipid rich atheromas (soft core), abundant inflammation, few smooth muscle cells mechanical stress (at the junction of fibrous cap and adjacent normal wall)
Extrinsic factors- adrenergic stimulationp upon awakening, emotional
Coronary thrombosis
partial or toral, superimposed on a partially stenosis plaque
Critical to the pathogenensis of acute coronary syndromes
Total occlusion –> acute transmural MI or sudden death
Incomplete occlusion mural thrombus- unstable angina, acute subendocardial infarction, sudden death, emboli (into more distal coronary artery)
vasoconstriction
comprises lumen size and increases mechanical forces that contributes to plaque rupture, leads to severe but transient reduction in coronary blood flow
Stimulated by (adrenergic agonists in circulation), locally released platelet contents, endothelial dysfunction leading to impaired secretion of endothelial relaxing factors, mediators released from mast cells
angina pectoris
paroxysmal and recurrent attacks of chest pain caused by transient myocardial ischemia, 15s to 15 mins, no cell necrosis
Three patterns- stable (produced by physical activity or emotional excitement, attributed to chronic stenosisng coronary AS
prinzmetal- due to coronary artery spasm at rest
Unstable- occurs with progressively increasing frequency and progressively less effort often at rest and of prolonged duration induceed by disruption of plaque with superimposed partial thrombosis, often prodrome of acute MI
MI
death of cardiac muscle due to ischemia, M>F (premenopausal)
Risk factors- increasing age and predisposition to atherosclerosis, HTN, cigarettes, DM, increased cholesterol and lipids
Pathogenesis- in 90%- acute plaqe change resulting in thrombosis and occlusion of coronary artery
in 10% cvasospasm emboli or unexplained
mi types
Transmural- full thickness of ventricular wall, confined to distribution of one vessel, fixed coronary obstruction with superimposed acute plaque change and complete obstructibe thrombosis
Sub endocardial- necrosis limited to inner 1/3, may extend laterally beyond perfusion of one vessel, fixed coronary obstruction with nonocclusive thrombosis or lysis of thrombus or hypotension
Myocardial response to MI
loss of contractility- 60s of ischemia may precipitate acute heart failure
Loss of blood supply–> reversible damage in early stages
20-40 mins–> irreversible damage (coagulative necrosis)
Early thrombolytic therapy 3-4 hrs–> reperfusion and limit size of infarct
arrythmias (induced by myocardial irritability secondary to ischemia/infarction- ventricular fibrillation0 –> sudden death
Classic biochem markers- CKMB, troponin, STEMI
myocyte injury
Cardiac injury is the disruption of normal cardiac myocyte membrane integrity resulting in the loss into the extracellular space including blood of intracellular constituents- TROPONIN (Ck myoglobin, heart type fatty acid binding protein, lactate dehydrogenase), injury is usually considered irreversible (cell death)
3-6 hours of AMI, peak 12 -16 remain elevated for a week,
hf and myocarditis both cause elevated troponins
Morphology of MI
LAD>RCA>LCA
<12 hours- not apparent, Tetrazolium stain- pale areas 2-3 hours post occurrence
12-24 hrs- dark red-blue mottling due to stagnant blood
1-14 days- Early (sharply defined yellow tan area), Late (still yellow-tan centrally but with hyperemic peripheral zone)
> 2 weeks- Gray white scar begins to form
MI histology
4-12 hrs- wavy fibers
12 hrs-7days - coagulation necrosis becomes well established and ongoing- initially pyknotic nuclei, hypereosinphillic myocytes, follwed by PMNs (1-3 days), loss of nuclei and striations, by 7 days macrophages at border
7-14 days- granulation tissue well established, collagen begins to deposit
> 14 days- progressively more collagen deposition eventually dense fibrous scar
