chap 8 Flashcards
coronary circulation
main blood supply of the heart
- myocardium is too thick for the diffusion of nutrients
- venous blood collected by cardiac veins
- empties blood into the RA
myocardial infarct
typically causes severe, persistent chest pain, often present atypically, may be asymptomatic
congestive heart failure
- fluid buildup in the lungs and other tissue s
- shortness of breath due to pulmonary edema
- edema in extremities
tests
chest x-ray, echocardiogram, electrocardiogram, serum enzyme levels, cardiac catheterization, stress test
congenital heart disease
atrial and ventricular septal defects
- mainfestations
- murmur
- easily fatigued
- heart failure
tetralogy of fallot
- rare: 5 in 10,000 infants
four heart defects
1) VSD
2) pulmonary stenosis
3) right ventricle hypertrophy
4) overriding aorta- aorta is between left and right ventricles, over VSD
manifestations
- aorta is between left and right ventricles, over VSD
- cyanosis
- slow growth
- heart failure
- variable life expectancy
treatment - surgery soon after birth
artherosclerosis
development begins early
- asymptomatic for many years
myocardial infarction
leads to necrosis of heart muscle from severe ischemia
- basic mechanisms that trigger ischemia
- sudden blockage of coronary artery from thrombus, blockage from atherosclerotic plaque, sudden greatly increased myocardial oxygen requirements
symptoms of acute myocardial infarction
- angina = severe, crushing, constrictive OR like heartburn
sympathetic nervous system response - GI distress, nausea, vomiting
- tachycardia and vasoconstriction
- anxiety, restlessness, feeling of impending doom
hypotension and shock - weakness in arms and legs
men vs women
may be asymptomatic
features of MI
50% MI occur without warning
50% preceded by episodes of angina
80-90% MI pateints arrive alive
- die before - cardiac arrhythmia
- minority recover without complications
- most develop clinical complications
myocardial infarction - diagnosis
medical history: inconclusive
- pain of severe angina may be similar to pain of MI
physical examination: usually not abnormal unless patient exhibits evidence of shock, heart failure, murmur
laboratory data of MI
electrocardiogram, ECG, or EKG
- enzyme tests; enzyme leak out from necrotic cells after an infarct
- the larger the infarct, the longer for elevated levels to return to normal
cardiac enzymes
creatine kinase, lactase dehydrogenase, troponin
diagnosis of MI
coronary angiogram to locate and determine degree of obstruction
treatment for CAD
treatment = destroy clot –> angioplasty
cardiac bypass
- stent
stent
brace lumen open
treatment for MI
control or eliminate risk factors
- cessation of smoking
- control of hypertension
- anti-coronary diet: low cholesterol and fat
- weight reduction
- exercise
clinical features of coronary heart disease
arrythmia, angina, ischemia, plaques, congestive heart failure, scarring, heart failure, myocardial rupture, ventricular aneurysm, cardiac arrest all related
long term complications of MI
arrhythmias, heart failure, cardiogenic shock, pericarditis, thromboemboli, cardiac rupture, ventricular aneurysm
hypertensive heart disease
hypertension leads to increased workload for the heart which leads to structural and functional changes
- manifestations
- enlarged heart
- heart failure
- ischemia
valvular heart disease
valvular dysfunctions:
valvular stenosis and valvular regurgitation
valvular stenosis
aortic stenosis, mitral stenosis
valvular regurgitation
aortic regurgitation, mitral regurgitation, tricuspid regurgitation
aortic stenosis
leaflets undergo degenerative changes –> fibrotic, calcified rigid –> restricts valve mobility, stenosis
clinical outcomes : increase strain, left ventricular hypertrophy –> heart failure
more common with aging
