| How is epidemiology of HTN? | HTN doubles risk of CVD (CHD, CHF, strokes, renal failure and periperal arterial diseases)
HTN increases with age 65% age >60 years.
Obesity and weight gain are strong independent risk factors to get HTN (60% HTN are 20% overweight), prevalence related to NaCl intake, low intake of Ca and K contributes to HTN, others (alcohol, psychosocial status, physical inactivity)
Blood pressure heritability is 15-35% high blood pressure before 55 occurs 3.7 times more if we have + fam hx |
| What are the determining factors of arterial pressure? | . |
| How is intravascular volume leading to HTN? | When NaCl intake exceeds capacity of kidney to excrete sodium, vascular volume expands and CO may increase (flow = pressure across vessels/resistance)
Initial increase of pressure is related to increased CO, but over time we get increased resistance and CO returns normal.
Also salt activates neural/endocrine/vascular mechanisms increasing arterial blood pressure.
Mechanism of pressure-natriuresis involves increase in GFR, decrease in absorbing capacity of renal tubules and hormonal factors like ANF, if pt with impaired capacity to remove sodium we get greater increase in BP to get normal natriuresis.
This could be due to renal disease/increased production of mineralocorticoids |
| How is ANS role in HTN? | Adrenergic reflexes modulate BP over short term, NE, EPI and DA play a role, receptors divided into (a1,a2,b1,b2) a1 postsynaptic cell in smooth muscles and elicit vasoconstrictors, a2 activated by catecholamines negative controllers inhibit further NE release.
b1 stimulates rate and strength of CO, and stimulates renin release from kidney, b2 EPI relaxes vascular smooth muscle results in vasodilation.
Sympathetic outflow increase in HTN than normotensive. |
| How is RAAS in HTN? | 3 stimuli for renin secretion (decreased NaCl in distal henle's loop, decreased pressure or stretch within renal afferent arteriole baroreceptors, sympathetic nervous system stimulation by b1 receptors)
Angiotensin type 1 (potent pressor, mitogen stimulates vascular smooth muscles and myocyte growth, role in pathogenesis of atherosclerosis)
Angiotensin type 2 (vasodilator, sodium excretion, inhibition of cell growth and matrix, improves vascular remodeling stimulating smooth muscle apoptosis, regulates GFR)
AT1 receptor blockade increases AT2 receptor activity.
Renin secreting tumors cause renin-dependent HTN, obstruction of renal arteries decrease renal perfusion stimulating renin secretion, excess AT2 contributes to atherosclerosis, cardiac hypertrophy and renal failure and maybe target to prevent organ damage.
increased RAAS doesnot mean HTN always, could be physio response/secondary aldosteronism not HTN, seen in edema/CHF/liver. |
| What are vascular mechanisms of HTN? | • In hypertensive patients， structural， mechanical， or functional
changes may reduce the lumen diameter of small arteries and arterioles
• Hypertrophic or eutrophic vascular remodeling results in decreased
lumen size and， hence， increased peripheral resistance.
• Vessels with a high degree of elasticity can accommodate an increase
of volume with relatively little change in pressure， whereas in a semirigid vascular system， a small increment in volume induces a relatively large increment of pressure |
| What are pathological consequences of HTN for heart? | • Heart disease is the most common cause of death in hypertensive patients
• Hypertensive heart disease is the result of structural and functional adaptations leading to left ventricular hypertrophy，
• Aggressive control of hypertension can regress or reverse left ventricular hypertrophy and reduce the risk of cardiovascular disease.
• Abnormalities of diastolic function that range from asymptomatic heart disease to overt heart failure are common in hypertensive patients. 1/3 of patients with CHF have normal systolic function but abnormal diastolic function |
| What are pathological consequences of HTN for brain? | • Stroke is the second most frequent cause of death in the world
• Elevated blood pressure is the strongest risk factor for stroke
• Treatment of hypertension decreases the incidence of both ischemic and hemorrhagic stroke
• Cerebral blood flow remains unchanged over a wide range of arterial pressures (mean arterial pressure of 50- 150 mmHg) through a process termed autoregulation of blood flow
• In patients with the clinical syndrome of malignant hypertension encephalopathy is related to failure of autoregulation of cerebral blood flow at the upper pressure limit， resulting in vasodilation and hyperperfusion. |
| What are pathological consequences of HTN for kidney? | • The kidney is both a target and a cause of hypertension.
• Primary renal disease is the most common etiology of secondary
hypertension.
• Mechanisms of kidney-related hypertension include (diminished capacity to excrete sodium, excessive renin secretion in relation to volume status, sympathetic nervous system overactivity)
• Hypertension is a risk factor for renal injury and ESRD
• Atherosclerotic， hypertension-related vascular lesions in the kidney
primarily affect preglomerular arterioles
• Clinically, macroalbuminuria (a random urine albumin/creatinine
ratio >300 mg/g) or microalbuminuria (a random urine albumin/
creatinine ratio 30-300 mg/g) are early markers of renal injury.
• These are also risk factors for renal disease progression and
cardiovascular disease |
| What are pathological consequences of HTN for peripheral arteries? | • Blood vessels are a target organ for atherosclerotic disease secondary
to long-standing elevated blood pressure
• Vascular disease is a major contributor to stroke， heart disease，
and renal failure
• The ankle-brachial index is a useful approach for evaluating PAD and
is defined as the ratio of noninvasively assessed ankle to brachial (arm) systolic blood pressure.
(An ankle-brachial index <0.90 is considered diagnostic of PAD and is
associated with >50% stenosis in at least one major lower limb vessel.
,An ankle-brachial index <0.80 is associated with elevated blood pressure，
particularly systolic blood pressure.) |
| How do we define HTN? | CVD risk doubles with each 20 mmHg increase systolic and 10 mmHg diastolic.
Systolic BP and PP are stronger indicators of CVD than diastolic, HTN is two or more seated BP readings during each of two or more visits. Nighttime BP 10-20% lower than daytime, an attenuated BP dip may be associated with increased CVD, criteria of dx std based on 24 h blood pressure monitoring, average awake BP >135/85 and asleep BP >120/75.
White coat HTN |
| Give table of HTN dx | . |
| How is clinical disorder of HTN? | 80-95% of pt have primary/essential HTN, 5-20% secondary.
Systolic HTN with wide PP (decreased vascular compliance atherosclerosis, increased CO [AR, Thyroctoxicosis, hyperkinetic heart, fever, fistula AV, patent ductus]) |
| What is primary HTN? | Familial, genetics and environment, spectrum of disorders underlying pathphysio, established HTN peripheral resistance is increased, and CO is normal or decreased. Younger pt mild/labile HTN, CO may be increased and peripheral resistance normal.
There is association between obesity and HTN direct correlation, 60% HTN pt are more than 20% overweight, adiposity attributes 65% of HTN, or insulin resistance
Metabolic syndrome (insulin resistance, abdominal fat, HTN, dyslipidemia) |
| What are secondary causes of HTN? | Renal (parenchymal diseases most common cause, 80% chronic renal failure pt, proteinuria >1000 active urine sediment indicate renal disease. Renovascular HTN [occlusive artery curable form of HTN, activated RAAS, at risk pt atherosclerotic and fibromuscular dysplasia, seen by contrast arteriography occluded >70% significant])
Endocrine (primary aldosteronism [curable HTN, sodium retention, HTN, hypokalemia, low plasma renin acitivity, refractory HTN. hypokalemic HTN due to seconday aldosteronims, PA/PRA useful, adrenal CT useful, scintigraphy last option] Cushing's [related to mineralocorticoid receptors by cortisol increase] Pheochromocytoma)
Miscellaneous causes (OSA , coarctation of aorta [most common congenital cause, diminished femoral pulse , therapy surgery/balloon angioplasty], thyroid disease and acromegaly, hyperPTH |
| How is approach to pt with HTN? | Hx (complete, PE confirm HTN, screen other CVD, secondary causes of HTN, cardiovascular consequences of HTN search, BP related lifestyles)
Labs (urinanalysis, albumin excretion, serum creatinine, serum ions, FBG, total cholesterol TGs, hematocrit, ECG)
Dx (algorithms) |
| How is tx of HTN? | lifestyle modification (BMI, salt reduction, DASH-type diet, moderate alcohol, physical activity) |
