Cardiopulmonary: Cardiovascular pathophysiology Flashcards
(44 cards)
Functional classification of heart disease
Atherosclerotic heart disease
- most common cause of CV disease
- more common in men than women
- characterized by irregular distributed lipid deposits in the intimal layer of medium and large Coronary arteries
Modifiable risk facors for atherosclerosis
- elevated total cholesterol
- high LDL/vLDLs
- low HDL
- high triglycerrides
- obesity
- HTN
- smoking/tobacco
- excessive alcohol
- physcal inactivity
Non-modifiable risk factors for atherosclerosis
- males
- age
- family history of CAD in male relative before 55 or female relative before 65
how does an atherosclerotic lesion occur
- abnormal lipid metabolism and/or excessive intake of cholesterol and saturated fats
- atherosclerotic plaque
- fatty streak
- fibrous plaque
- atherosclerotic plaque: accumulation of intraellular anad extracellula lipids, connective tissue, smooth muscle cells, and glycosaminoglycans
- fatty streak: first detectable lesion; consists of lipid-laden foam cells
- foam cells: macropahges that have mirgated as monocytes from circulation into subendothelial layer of the intima
Describe the lipid hypothesis: pathogenesis
- increased LDL levels result in penetration of LDL into the arterial wall
- leads to lipid accumulation in smooth muscle
- fatty streak evolves into fibrous plaque
Describe chronic endothelial injurry hypothesis
- Endotheliam injury
- over time the plaque becomes calcified
- some plaques are stable but others may spontaneously fissue and ruptutre
- ruptured plaques stimulate thrombosis
Endotheliam injury produces loss of endothelium, adhesions of plateletes to subendothelium, aggegation of plateletes to subendothelium, aggrergation of plateletes, chemotaxix of monocytes, and T-cell lymphocytes + release of platelet-derived and monocyte derived growth factors
What happens when a plaque ruptures
- may emobilize
- rapidly Occlude the lumen/cause MI or infarcation
- gradually becomes incorporated into the plaque
What is myocardial ischemia
- results with an imbalane between O2 supple and demand
- revesible
- comforable at rest and symptoms during mild-moderate exercise
What is stable angina
- classic symptom= angina pecoris (heaviness, pressure or tightness in chest)
- may be precipitated by exertion, stess, emotion, heavy meals
- lasts for several minutes
- relieved by rest and nitroglycerin
What is unstable angina
- change in angina pattern or angina at rest
- may last longer ot not respond
- typically caused by plaque rupture, ulceration or hemorrhage with subsequent thrombus forrmation
What is prinzmeta angina
- unusual type of angina that occurs mostly at rest
- hypothesized that it is the result of transient increase in vasomotor tone or due to vasospam
- assoicated with ST elevation rather than depression on EKG
- may be assoicated with acute MIs, severe arrhythmias (Ventricular tachycardia or fibrillation)
Asymptomatic/silent angina
- Angina that is asymptomatic
- factors include age, presence of CAD, or other disease process
- pts with DM have a high incidence of painless MIs and definite silent ischemia
What are angina equivalents
- dyspnea
- fatigue
- lightheaded
- beltching brought on by exercise and relieved with rest or nitro
What is the pathogenesis of a MI
- results from prolonged ischemia
- almost always in the left ventricle
- tissues become necrrotic in zone of infarction
- formation of fibrous scar within 6-8 weeks (inelastic)
What is a transmural MI
- full thickness necorsis
- wall motion reduced (hypokinetic), abnormal (dsykinetic) or absent (akinetic)
What is the zone of hypoxic injury
area where tissue may be able to return to normal but may become necrotic if blood flow is not restored
How is an MI diagnosed
must have 2/3
- hx of ischemic type chest discomfort
- evolulationary changes on serially obtained ECG
- rise and fall in serum cardiac enzymes
Clinical presentation of MI
- crushing chest pain or pressure
- may radiate to arms, neck, throat/jaw, and back
- pain is constant and lasts >30 minutes
- pallor/SOB
- unrelieved pain w/ 3 doses of nitro
- diaphoresis
- nausea/vomitting
- Denial
Diagnosis of MI via ECG
- peaked T-waves following
- ST-segment elevation
- q-wave development
- and finally T-wave inversion
Diagnosis of MI with cardiac enzymes
- creatine kinase (MB specific to myocardium)
- myoglobin
- cardiac specific troponin
- lactic dehydrogenase
- serum glutamic-oxaloacetic transaminase
CK-MB will increase with 4-8 hours and retunr to normal withiin 2-3days
Treatments of MI
Medical: pharmocologic agents to
- decrease O2 demand
- increase O2 supply
- improve or maintain myocadial function
Surgical:
- thrombolysis
- intra-aortic ballon pump
- angioplasty and stent placement
some drugs that dissolve a thrombus (lysis) may be delievered surgically via catheter
What determines systolic dysfunction
- end-diastolic volume/preload
- afterload
- contracile state of myocardium (contractility)
- heart rate (chronotrophy)
heart function may be impaired as a esult in alterations of any four of these
What is predominant distolic dysfunction
- filling of ventricle is impaired due to hypetrophy or changes in myocardium composition