lecture notes Flashcards
circulation pathways
pulmonary
cardiac
systemic
stroke volume x heart rate =
cardiac output
SNS
↑ HR, cardiac contractility, tension of blood vessels
PNS
↓ HR
atherosclerosis
lipid deposits on lining of arteries
causes of atherosclerosis
injury to lining
- HTN, smoking, environmental exposure
thrombosis
clot due to vessel wall damage/ turbulent of stagnant flow
hypercoagulability
excessive clotting
causes of hypercoagulability
congenital or acquired
autoimmune, cancer, myeloproliferative disorders (thrombocytopenia), sickle cell disease, polycythemia vera, oral contraceptives, vascular changes in late stage of pregnancy
thrombus
blood clot w/in vascular system that impedes flow of blood
embolus
any plug of material (thrombi, air, neoplasm, microorganism, amniotic fluid) that travels and can obstruct the lumen of a vessel
thromboembolus
blood clot that breaks off and travels
infarct
area of necrosis resulting from insufficiency of blood supply - results in loss of function of affected tissue
infarction
process of obstructing a vessel
classifications of shock
cardiogenic
hypovolemic
massive system vasodilation
causes of cardiogenic shock
MI is leading cause
any condition that leads to inefficiency
causes of hypovolemic shock
hemorrhage
burns
diarrhea
polyuria - like in DI
massive systemic vasodilation
septic
neurogenic
anaphylactic
s/s of shock
chest pain, SOB, labored breathing, diaphoresis, N/V
risk factors of MI
family hx, HTN, smoking, cholesterol levels, comorbid DM
MI
total occlusion of coronary arteries
results in ischemia/death of myocardial tissues
cause of MI
atherosclerosis
heart failure
heart is unable to maintain blood circulation/meed demand of tissues and organs
HF causes
secondary to other conditions
MI, heart defects, infection, HTN, inflammation of heart tissue, fluid volume overload, anemia
L sided HF s/s
fluid in lungs - pulm edema
bilat rhonchi/crackles in base
R side HF causes
L sided HF
lung injury
infections
inflammation
pulm edema
types of lipids
triglycerides
phospholipids
steroids
triglycerides
major storage form of fat in body
important energy source
phospholipids
essential to building plasma membranes
steroids
cholesterol is most known
building blocks of biochemicals: vitamin D, bile acids, cortisol, estrogen, progesterone, testosterone
lipoproteins
transport lipids through bloodstream
LDL
major contributor to CAD
leads to plaque buildup and atherosclerosis
decreasing LDL decreases incidence of
CAD
HDL
interacts w bile and excreted into feces
hyperlipidemia
high levels of lipid
hypercholesterolemia
form of hyperlipidemia
abnormal levels of lipoproteins
causes of hyperlipidemia
diet high in saturated fats, trans fats, refined carbs
lack of exercise
inherited or acquired
diuretic
furosemide
↑ urine output = ↓ fluid volume
ACE inhibitor
- rils
lisinopril
block formation of angiotensin II = vasodilation and block aldosterone secretion = ↓ fluid volume
angiotensin receptor blocker
“arbs”
losartan
prevent angiotensin II from reaching receptors = vasodilation
calcium channel blockers
nifedipine, diltiazem
block calcium ion channels in arteries = vasodilation
beta-adrenergic antagonists - beta blockers
atenolol
↓ HR and myocardial contractility = ↓ cardiac output
alpha 1 adrenergic antagonists - alpha blockers
doxazosin
inhibit SNS activation in arterioles = vasodilation
alpha 2 adrenergic agonists
clonidine
↓ SNS impulses to heart and arterioles = vasodilation
direct acting vasodilators
hydralazine
act on smooth muscle of arterioles = vasodilation
