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
Hypercortisolism clinical signs
Elevated blood sugar, HTN, central obesity with peripheral wasting, buffalo hump, moon facies
Mechanism of hypercortisolism-induced HTN
Cortisol and aldosterone are almost identical in structure - glucocorticoids have a varying effect on mineralocorticoid receptors
Cushing’s syndrome
Excessive cortisol
Cushing’s disease
Excessive cortisol secondary to pituitary ACTH hypersecretion resulting in adrenal hypersecretion of cortisol
Coarctation of the aorta
Narrowing of aorta > BP lower in legs than arms
Hyperthyroidism mechanism of HTN
- Increased expression of beta receptors resulting in increased sensitivity to catecholamines > increase contractility and HR, increase sympathetic tone to increase TPR
- Thyroid hormones stimulate Na/K pumps in kidney > increase Na and H2O resorption
Hyperthyroidism clinical signs
Palpitations, exophthalmos, weight loss, goiter
Viscerosomatic reflexes for heart and kidney
Heart: T1-5, vagus
Kidney: T10-L1, S2-4
Heart Chapman’s
Anterior: medial 2nd intercostal
Posterior: T2 transverse processes
Kidney Chapman’s
Anterior: 1” superior and 1” lateral to umbilicus
Posterior: L1 transverse processes
Adrenals Chapman’s
Anterior: 2” superior and 1” lateral to umbilicus
Posterior: T11 transverse processes
Absolute compelling indication
Compelling indication is the requirement for a certain antiHTN drug class(es) for a condition
Relative compelling indication
Compelling indication is suggestion for a certain antiHTN drug class(es) for a condition
Absolute compelling contraindication
Requirement to NOT use a certain antiHTN drug class(es)
Relative contraindication
Condition which makes a particular treatment or procedure potentially inadvisable
Options for drugs for pregnancy
Methyldopa, hydralazine, vasodilators, labetolol
relative indications for thiazide diuretics
Osteoporosis
Absolute contraindications for thiazides
Hypokalemia
Relative contraindications for thiazides
Gout
Absolute indications for BB
CVD, HF
Relative indications for BB
atrial flutter/afib
Absolute contraindications for BB
2nd or 3rd degree block, bradycardia
Relative contraindications for BB
Fatigue, depression, aggravate asthma
Absolute indications for ACEI/ARBs
CKD stage 1-3b, CVD, HF
Absolute contraindications for ACEI/ARBs
pregnancy, bilateral RAS, hyperkalemia, AKI
Relative contraindications for ACEI/ARBs
CKD stages 4-5
Relative indications for CCB
African-American, afib/flutter (non-dihydropyridine)
Absolute contraindications for CCB
2nd or 3rd degree block, bradycardia (non-dihydropyridine), systolic HF (non-dihydropyridine)
Relative contraindications for CCB
Systolic HF (dihydropyridine), edema, fatigue
Indication for aldosterone antagonises/K sparing diuretics
Add-on to thiazide that causes hypokalemia
Absolute contraindications for aldosterone antagonists/Ksparing diuretics
Hyperkalemia
Resistant HTN
Persistence of HTN despite concurrent use of adequate doses of 3 antiHTN agents from different classes (including diuretic)
Causes of resistant HTN
- Meds (alcohol, NSAID, illicit drugs, OCP, steroids, decongestants, licorice, ephedra
- Secondary causes of HTN
Causes of pseudo-resistant HTN
- non-compliance provider is unaware of
- improper BP measurement
- volume overload
First-line agents for HTN
Diuretics, ACEI, ARBs, renin inhibitor, CCB, BB (no longer used for initial therapy in absence of specific indication)