Cardiac Diseases Flashcards
Heart layers [review]
epicardium = outer surface myocardium = middle, muscular contracting layers endocardium = inner, lines the inner chambers and heart valves
Heart valves [review]
AV valves: bicuspid (mitral) on the left, tricuspid on the right.
Semilunar valves: pulmonic (RV and pulmonary arter) and aortic (LV and aorta)
Cardiac Conduction [review]
SA node (pacemaker) (60-100BPM) to
Right and Left Atria to
AV node (50BPM if SA stops working) to
Bundle of His (40BMP if others dysfxn) to
Right and Left bundle branches to
Purkinje Fibers (ventricular contraction)
1st heart sound [review]
“Lub” - AV valves shut at the beginning of systole - sound is the interruption of laminar flow (blood against a closed valve)
2nd heart sound [review]
Semilunar valves shut at the end of systole d/t falling pressure
- *physiologic split** = artic valve closes earlier than pulmonic by .02-.04 seconds in exp, and .04-.06 in insp - helps sides keep together
- – pulmonic opens sooner, closes later
Atherosclerosis
- *most commonly on coronary arteries - or other larger vessels
- hardened plaque - fibrofatty lesions internally lining vessels
- most common cause of CAD = inflammation from ATO
- progression of ATO means vessel can’t dilate as well
- advanced: calcification or rupture
Atherosclerosis: inflammation
Deposits attract bacteria and then inflammatory response.
- Same risk factors of HD initiate chemical response for inflammation (smoking, HTN, lipoproteins, hyperglycemia)
Organisms that could contribute to atherosclerosis
chlamydia pneumoniae, Herpes simplex virus, Cytomegalovirus
Atherosclerosis: r/t morbidity and mortality
- responsible for most cases of MI and CVA
- Principle cause of death in the US and Western Europe
- Potential sequelae: MI, CVA, gangrene in extremities, sudden cardiac death
Atherosclerotic Lesion dvlpmt: fatty streaks
- occurs in all ages.
- kids at 1-2yo, if homozygous dominant for hypercholesterolemia
- Contains foam cells: T cells and macrophages filled with lipids
- results in disorganized layers of cells: smooth muscle from tunica media migrates into tunica intima
Atherosclerotic Lesion dvlpmt: Fibrous Plaques
- CT, smooth muscle cells full of lipids, macrophages, lymphocytes
- thickens and may occlude the lumen, often w/ necrosis and calcification
PROCESS: Plaque expands => Artery gets inflamed => fibrous capsule forms => separates plaque from lumen => decreased blood flow, increased BP
Atherosclerotic Lesion dvlpmt: Complicated lesion
- Degenerated plaque may rupture
- Softer lesions more likely to rupture
- Ulcerations, cracks serve as sites for platelet adherence and aggregation. Can result in thrombus => occlusion => MI
Common Sites of Atherosclerosis (list)
(All Arteries)
- Aorta
- Femoral A
- Popliteal A
- Tibial A
- Coronary As
- Carotid As
- Cerebral As
Common Sites of Atherosclerosis (description)
- more common at bifurcations where there is more force
- In legs: more common w/ DM or smokers
- In coronary As: more common in epicardial portions
- New lesions may occur at sites of CABG b/c tissue is less smooth after surgery
Atherosclerosis: risk factors
- Males over 45, Females over 55 or early menopause
- Family Hx of premature CHD, AMI, Sudden death
- HTN
- High LDLs/ Low HDLs
- High triglycerides
- DM
- Obesity & inactivity
- Low birth weight
Atherosclerosis risk factors: Hyperlipidemia
( high levels of fats in blood)
- Clear assc. w/ CAD and Hypercholesterolemia
- risk increases with high LDL cholesterol
- cause: dietary, genetic, overproduction, deficient removal, DM, renal disease, alcoholism, hypothyroidism, corticosteroids, estrogens….
Atherosclerosis risk factors: Smoking
- Accelerates Ath
- 3-5x risk of CAD
- 70% death rate
BUT! Cessation lowers risk to that of non-smokers within ONE YEAR.
Atherosclerosis risk factors: Diabetes Mellitus
Basically, metabolism of fat is affected.
- 4x risk of MI
- risk of gangrene in LE
- females more prone
- often hand in hand w/hyperlipidemia
- Goal: control blood sugar and BP
Atherosclerosis risk factors: Hypertension
can be a silent killer
- Risk 5x greater when 160/95
BUT: this is the MOST TREATABLE aspect of the disease
Atherosclerosis risk factors: Obesity and inactivity
Obesity assc w/ hypertriglyceridemia, hypercholesterolemia, glucose intolerance, HTN
Inactivity may lower HDLs
Coronary Artery Disease: mortality and risk
- leading cause of death and disability in the US
- 1/3 males, 1/10 females under 60 - post menopause =
- 800000 new AMIs yearly
- 540,000 recurrences yearly
- BUT! Mortality is declining d/t:
- CPR and better hospital care
- management of HTN
- Lower cholesterol diets
- use of antibiotics
Manifestations of CAD: Sudden Cardiac Death
- w/in an hour
- first sign of trouble in 25% of cases
- 350,000 deaths annually
- peaks for infants (born with heart defects) and adults 45-75
- more frequently in the AM
Sudden Cardiac Death: Causes
90% direct result of lethal dysrhythmias: V tach, V fib, bradycardia, asystole
Major factors:
- 75% d/t CAD
- 25% d/t myocardial abnormalities (hypertrophy, dilation, valvular disease)
Occurs with:
- 75% or greater narrowing of Coronary As (stent needed)
- Old AMI
- acute thrombosis at site of fissured plaque
- note: 90% of Carotid cases: no symptoms until 90% narrowing d/t circle of willis
SCD: treatment
if untreated, irreversible brain damage in 3-5 minutes and death
Treatment:
- CPR
- defibrillation, pacing for bradyarrhythmia, drugs
- Electrophysiologic testing to ID drug therapy needed
- implanted cardioverter/defibrillator
- resection of diseased myocardium
CAD: description
- atherosclerosis narrows/obstructs the coronary As
- Decreased perfusion of myocardial tissue, inadequate O2 supply
CAD: outcomes
- Symptoms occur when there is inadequate blood supply (ischemia)
- L. main artery = “widowmaker.” CAD significant if occlusion is reduced 50% here, or 75% in any other major branch.
- Leads to: HTN, angina, dysrhythmia, MI, CHF, death
CAD: Collateral circulation
CC = more than one artery supplies a muscle with blood.
- present in coronary As (especially in older folks)
- but it takes time to develop
- CAD in younger people is more likely to be lethal!!
CAD: Treatment
Treat the underlying condition.
- Occlusion more than 70% requires a stent
- Patients may go to cardiac rehab to help develop collateral circulation
Angina: description
- Chest pain from myocardial ischemia
- caused by imbalance b/t O2 supply and demand
- provoked by exertion or anxiety
- lasts several minutes, alleviated by rest.
- No myocardial necrosis (cells are HUNGRY not dead)
- Sequelae: AMI, death
Angina: Oxygen supply and demand
- Symptoms occur when O2 demand > supply
- Determinants of O2 demand: HR, contractility, Ventricular wall tension
- also physiological states increase demand: exercise, emotional stress, increased SNS activity
