principal determinants of BP - arterial pressures (CO X peripheral resistances) and Cardiac outputs
(heart rate, myocardial contractility, blood volumes and venous returns)
life style modifications available to tx hypertension - weight loss, sodium regulations, DASH diets,
alcohol restriction, a...
principal determinants of BP - arterial pressures (CO X peripheral resistances) and Cardiac outputs
(heart rate, myocardial contractility, blood volumes and venous returns)
life style modifications available to tx hypertension - weight loss, sodium regulations, DASH diets,
alcohol restriction, aerobic exercises and smoking cessation
consequences of hypertension - myocardial infarction, heart failure and angina development,
kidney disease risk, stroke and arterial pressure rising
hypertension - most prominent risk factor in developing cardiovascular disease, BP increases as
we age which puts everyone at risk for development
normal blood pressure - systolic <120mmHg and Diastolic <80 mmHg
stage 2 hypertension blood pressure - systolic and diastolic are in different categories (systolic 160
and above while diastolic is 90 and above)
primary (essential) hypertension - no identifiable cause, progressive and lifelong disorder; there
are treatments available but no cure
populations at risk of primary hypertension - older adults, african americans, mexican/hispanic
background, postmenopausal women, obese patients
,secondary hypertension - Identifiable cause (usually due to another illness), possibility to treat
cause directly which can "cure" the patient
how is arterial pressure measured? - cardiac output x Peripheral resistance
the direct benefits of lowering blood pressure will - decrease the individual from the risk of heart
disease
systems that regulate BP - sympathetic baroreceptor reflexes, RAAS, renal regulation
decreases in BP will cause activation of - sympathetic nervous system and vasopressin release
activation of sympathetic nervous system due to a decrease in BP will cause - increase in renin
release and activation of smooth muscles to increase HR and TPR
renin release due to sympathetic nervous system stimulation will activate - angiotension I which
will then activate angiotension II to effect the kidney and increase volume production
retentions of water and sodium will lead to - increases in blood volume and ICF
B-blockers and peripherally acting sympatholytics cause effects to which organ? - The heart
(decreasing force and rate of contractions); decreases CO
diuretics, angiotensin inhibitors and B-blocks cause effects to which organ - Kidney; decreasing
blood volume (decreasing CO)
peripherally acting sympatholytics, CA++ channel blockers, direct vasodilators and angiotension
inhibitors cause effects to which organ? - Vascular smooth muscles; relaxation of SM (decreases
TPR)
, centrally acting sympatholytics and B-receptor blockers cause effects to which organ? - Brain;
decreases sympathetic outflows (decrease CO AND TPR)
calcium channel blockers overall effects - decrease TPR, reflex tachycardia, no effects on CO or
plasma volumes
verapamil/nifedipine MOA - inhibit influx of ECF calcium across myocardial and vascular smooth
muscle cells; dilation of coronary and systemic arteries
verapamil/nifedipine use - lowering BP, angina
side effects of verapamil - sinus bradycardia, AV block
Why is there no reflex tachycardia in verapamil use - directly slows HR down due to the types of
calcium channels it blocks
nifedipine side effects - AV block, reflex tachycardia
why does reflex tachycardia occur with nifedipine? - dilation of coronary and systemic arteries
results in reflux
how do calcium channel blockers work within cardiac myocytes - calcium enters into sarcoplasmic
reticulium which connects with actin-troponin C and myosin; results in cardiac muscle contraction
B-AR blockers overall effects - decreases HR, CO, SV and plasma renin; no changes in plasma
volume or TPR
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