HTN Flashcards
What do you do to treat Stage 1 HTN?
- If ASCVD risk is <10%, just healthy lifestyle
- If ASCVD risk >10%, both lifestyle modification and one med
- If pt has known CVD, DM, or CKD, then lifestyle modification and one med
What do you do to treat Stage 2 HTN?
2 meds + healthy lifestyle
What magic number does CV risk start to increase?
Anything beyond 115/75
Criteria for diagnosing HTN 18 years and older
- Avg of 2 or more BP measurements on separate days
- Based on EITHER systolic or diastolic
- Office BP of 130/80 or higher
Criteria for diagnosing HTN in children/adolescents
- Avg of 2 or more BP measurements on separate days
- Based on EITHER systolic or higher
- BP at or above 95% for age, height, and gender
What’s the biggest modifiable risk factor for ASCVD?
HTN
Primary HTN
HTN with NO identifiable cause, NO cure, most cases
-gradual increase with slow rate of rise in BP, lifestyle factors that favor high BP, family hx of HTN
Secondary HTN
HTN with cause, correction of cause may cure the HTN, very few cases
NML BP
Elevated BP
Stage 1
Stage 2
<120/<80
120-129
130-139 OR 80-89
>140 OR >90
BP = …
CO * TPR
CO = …
SV * HR
How is HTN maintained
HTN > heart releases ANP > vasodilation and increase in Na and H2O excretion > kidney senses low pressure > release of renin > angiotensinogen to ang 1 > ACE converts ang 1 to ang 2 > aldosterone released and vasoconstriction > kidney reabsorbs Na and water > HTN
Secondary causes of HTN
Sleep apnea, RAS, CKD, hyperaldosteronism, pheochromocytoma, coarctation of aorta, hypercortisolism, hyperthyroidism
Most common secondary cause of HTN
Sleep apnea
What’s the mechanism for sleep apnea leading to HTN?
Repeated arterial desaturation sensitizes the carotid body chemoreceptors causing sustained sympathetic over-activity even during waking hours
Clinical signs of sleep apnea
Snoring, tired, observed apnea, elevated BMI, >50 yo, enlarged neck circumference, male
RAS causes and s/s
- atherosclerosis, fibromuscular dysplasia
- renal a bruit, classic worsening renal fxn with ACEI or ARB
RAS mechanism for HTN
- unilateral RAS causes underperfusion of JG cells > RAAS
- bilateral RAS causes renal failure and volume-dependent HTN
CKD cause and s/s
- expanded plasma volume d/t lack of capacity to excrete Na and H2O > RAAS
- asymptomatic edema, HTN, flank pain, and/or decreased urine output
Hyperaldosteronism causes
- Primary: unilateral aldosterone-producing adenoma (Conn’s) and bilateral adrenal hyperplasia
- Secondary: renin-secreting tumor, HF, cirrhosis, black licorice
Pheochromocytoma P’s
- paroxysmal pressure
- pain headache
- palpitations
- pallor
- perspiration
Mechanism of increased HTN via pheo
- Stimulates alpha1 receptors to increase vasoconstriction
- Stimulates beta1 receptors to increase HR and contractility in heart and increases renin release in kidney
- Stimulates beta2 receptors to increase smooth muscle relaxation in airways
Why do you also have to get phenoxybenzamine with beta-blockers?
Only beta-blockers would give unopposed vasoconstriction since it doesn’t affect alpha receptors