NSG 533 EXAM 3
Blood pressure formula
BP = CO (cardiac output) x SVR (peripheral resistance)
Cardiac output formula
CO = HR x SV
-preload
-contractility
-after load
-autonomic effects
-humoral effects
Primary hypertension
90% cases; no clear etiology
Two main contributors
1. vasoconstriction effect on SVR (obesity, inflammation, insulin resistance)
2. Na/H2O retention effect on blood volume(natriuretic dysfunction, RAAS/SNS)
,Hypertension impact
-Contributes to heart disease, #1 killer, and stroke, #5 killer
-$150-200b/year
-Leading social inequity/disparity
Secondary hypertension
Rare; established etiology and reverses once underlying disease is fixed
-neuro/renal/endo disorders/failure/tumors
-pregnancy induced
-acute stress, drugs
Primary hypertension risk factors
Family
Age (men<55, women>70)
Black
Sodium
Diabetes
Smoking
Obesity/poor nutrition
Alcohol
, Modifiable HTN risk
Smoking, alcohol, diet, obesity, stress
Nonmodifiable HTN risk
Genes, insulin sensitivity, SNS/RAAS activity, cellular mechanism, race
Hyaline sclerosis vs Atherosclerosis
hyaline: glass-like protein accumulation due to age
Athero: accumulation of arterial plaques
Pressure-Natriuresis effect on HTN
Right shift in urine sodium excretion and arterial pressure curve; requires higher
pressure to excrete salt
Renin-Angiotensin Aldosterone effect on HTN
1. Overactive ACE/Angiotensin II/At 1 system
2. Underactive At2, MAS receptor
SNS effect on HTN
Vasoconstriction = increased SVR = sustained HTN = remodeling
Metabolic effect on HTN
Adipose cells secrete leptin and inhibit adiponectin = trigHTN pathway
Blood pressure formula
BP = CO (cardiac output) x SVR (peripheral resistance)
Cardiac output formula
CO = HR x SV
-preload
-contractility
-after load
-autonomic effects
-humoral effects
Primary hypertension
90% cases; no clear etiology
Two main contributors
1. vasoconstriction effect on SVR (obesity, inflammation, insulin resistance)
2. Na/H2O retention effect on blood volume(natriuretic dysfunction, RAAS/SNS)
,Hypertension impact
-Contributes to heart disease, #1 killer, and stroke, #5 killer
-$150-200b/year
-Leading social inequity/disparity
Secondary hypertension
Rare; established etiology and reverses once underlying disease is fixed
-neuro/renal/endo disorders/failure/tumors
-pregnancy induced
-acute stress, drugs
Primary hypertension risk factors
Family
Age (men<55, women>70)
Black
Sodium
Diabetes
Smoking
Obesity/poor nutrition
Alcohol
, Modifiable HTN risk
Smoking, alcohol, diet, obesity, stress
Nonmodifiable HTN risk
Genes, insulin sensitivity, SNS/RAAS activity, cellular mechanism, race
Hyaline sclerosis vs Atherosclerosis
hyaline: glass-like protein accumulation due to age
Athero: accumulation of arterial plaques
Pressure-Natriuresis effect on HTN
Right shift in urine sodium excretion and arterial pressure curve; requires higher
pressure to excrete salt
Renin-Angiotensin Aldosterone effect on HTN
1. Overactive ACE/Angiotensin II/At 1 system
2. Underactive At2, MAS receptor
SNS effect on HTN
Vasoconstriction = increased SVR = sustained HTN = remodeling
Metabolic effect on HTN
Adipose cells secrete leptin and inhibit adiponectin = trigHTN pathway
