Pathophysiology of HTN Flashcards
key steps for proper BP measurements
- properly prepare the pt
-rest quietly for ~5 min
-pt should be relaxed, sitting, both feet on floor, remove clothing under the cuff, no recent caffeine or smoking - use proper technique for BP measurements
-BP cuff size should be appropriate
-use an upper arm measurement, around the level of the heart/right atrium - take the proper measurements needed for dx and tx of elevated BP/HTN
- properly document BP readings & average multiple readings
normal blood pressure
SBP < 120 AND DBP < 80
elevated blood pressure
SBP 120-129 AND DBP < 80
stage 1 HTN
SBP 130-139 OR DBP 80-89
stage 2 HTN
SBP 140+ OR DBP 90+
primary (essential) HTN - defined
*unknown cause
*likely genetic & environmental influences
secondary HTN - defined & when to suspect it
*due to an identifiable cause
*consider secondary HTN if…
-refractory or resistant HTN
-young age of onset (<30 in adults)
-associated hypokalemia
-abrupt onset or significant increase in HTN in a short period of time
-very severe HTN
refractory/resistant hypertension - defined
*blood pressure that is still not at goal despite treatment with 3 medications at max tolerated dose, all from different classes, including a diuretic
hypertensive urgency vs. emergency
*both have severe HTN: BP 180/120 or higher
*HTN urgency: no end organ damage
*HTN EMERGENCY: SIGNS OF END ORGAN DAMAGE:
-pulmonary edema
-papilledema, ICH
-MI/elevated troponins
-AKI
-aortic dissection
white coat hypertension - defined
*HTN only seen in doctor’s office
*normal BP at home, however, pt is more nervous in medical setting, so blood pressures are higher
*this can be confirmed with 24h ambulatory BP monitoring
masked hypertension - defined
*opposite of white coat HTN
*blood pressure is NORMAL in the doctor’s office but runs HIGH AT HOME
*detected through 24h ambulatory BP monitoring
lifestyle interventions to treat HTN
*WEIGHT LOSS
*heart healthy diet (ex. DASH diet)
*low salt diet
*exercise/increased physical activity
*decrease alcohol consumption
*treatment of OSA with CPAP
suspected pathogenic mechanisms in HTN
- abnormal kidney handling of sodium & plasma volume
- activation of sympathetic nervous system
- activated RAAS
- likely other environmental & genetic factors
effects of abnormal kidney handling of sodium & plasma volume → HTN
*excess Na+ (and thus excess water) content in blood → higher blood pressure
pressure natriuresis
*mean arterial pressure increases as sodium intake increases
*2 clinical categories:
1. salt sensitive:
-more likely to respond to diuretic and dietary salt restriction
-have lower renin levels
2. salt insensitive:
-more likely to respond to RAAS blockade
-have higher renin levels
effects of RAAS → HTN
angiotensinogen → angiotensin I → angiotensin II → aldosterone
*end result = INCREASED BLOOD PRESSURE / VOLUME
*rate limiting step = RENIN RELEASE (recall: renin converts angiotensinogen to angiotensin I)
angiotensin II - effects leading to increased blood pressure
*sodium reabsorption
*water reabsorption (increased ADH)
*vasoconstriction
*increased sympathetic tone
*increased salt appetite
*increased thirst drive
end result: increased BP/blood volume
aldosterone - effects leading to increased blood pressure
*salt reabsorption → increased blood volume
*potassium excretion
*acid excretion
end result: increased BP/blood volume
factors that cause renin release
*decreased renal perfusion (systemic hypotension or low afferent arteriole pressure)
*increased sympathetic activity/tone
*decreased flow through tubules or decreased distal Na+ delivery (detected by macula densa)
*beta1 adrenergic stimulation
*low sodium diet
effects of aldosterone in the principal cell in the collecting duct
aldosterone (made by adrenal cortex) binds mineralocorticoid receptor (MR) inside principal cells → increased activity of Na+/K+ ATPase AND increased activity of ENaC → increased reabsorption of sodium into blood & wasting of potassium in urine
