Cardiac Function Flashcards
Cardiovascular disease (CVD)
Coronary heart disease (CHD)
Cerebrovascular disease
Peripheral arterial disease (PAD)
aortic atherosclerotic disease
CHD
Chest pain
Myocardial infarction
heart failure
Cerebrovascular disease
blood supply cut off from the brain
stroke or mini stroke
PAD
Blockage in the arteries to extremeties, usually legs
PAD and DVT (deep vein thrombosis)
Aortic atherosclerotic
Aneurysms and dissection
Atherosclerosis
Chromic inflam disease w/ accumulation of lipid material in the veins and arteries. cases narrowing and hardening.
Most common locations
Right coronary artery
Right marginal artery
Left decending artery
Left coronary artery
Acute coronary syndrome (ACS)
chest pain
Angina
missed in about 1% of patients
Angina
classic symptom of ischemia
Squeezing of the chest, radiates to left arm or shoulder and neck, gets worse with stress
Nonclassical symptoms more common in women
stabbing pain, viselike pressure. nausea, shortness of breath, ab pain
Markers of initial cardiac damage
Cell death releases proteins
Ideally: sensitive and specific, persist for several days, detectable in low concentrations
Creatine Kinase
Cardiac biomarker
CK - Creatine kinase
Exceeed range in 6-8 hours
peak at 24 hours
return to range in 3-4 days
CK-MB is most reliable
Cardiac Troponins
Complex or 3 proteins responsible for muscle contractions
TnT: binds to tropomyosin
TnI: inhibits binding of actin and myosin
TnC: Binds to Ca to reverse TnI. specific for cardiac damage
Measuring cTnT
Use monoclonal antibodies to detect
sensitive and specific
detectable 3-12 hours after onset, peak at 12-24, elevated for more than a week
hs-CtnT
Rise and fall indicate acute myocardial injury
CV <= 10%
Can be interfered with from other diseases that cause MI
Kidney disease and cardiac disease
CKD - increased Trop levels
Dialysis increases cTnT
Hemodialysis filters and alters concentrations of markers
Myoglobin
half life of 9 minutes
present in all muscle tissues
not specific and hs-Tn faster
Cardiac Injury
Myocyte death
Apoptosis to necrosis
Apoptosis requires energy. Necrosis occurs if energy supply fails
Treatments
Intravascular balloons and stints
CABG
Tissue plasminogen activator
Heart Failure
Fails to adequately supply
Manifested: Retention of fluid, shortness of breath, fatigue, lower extremely edema
Releases BNP and NT-proBNP - Hearts response to pressure/vol load
NT-proBNP and BNP
released by myocardial cells
strong predictor in people w/ heart failure
BNP target fro drug manufacturers
CHD risk
MPO and CRP indicate infalm response
MPO increased in ACS and CAD
CRP
Inflam marker
rapid synth in liver
hs-CRP
More sensitive than CRP
marker of choice for CHD risk
homocystine
Sulfuric AA
4 forms in blood
Connected to vascular disease
Hyperhomocysteimia linked with CVD
every 5umol increase correlates to 20-30% increase risk of ischemic heart disease
Pulmonary embolism
Circulating solid, liquid, or gas
Pulmonary arteries blocked
Risk increased for women - oral contraceptives.
treatment with anticoagulants effective
Saddle embolism
bifurcation blocked
60% blockage
