hypertension Flashcards
describe the hypertension blood pressure profile before and after 50
- Systolic and diastolic blood pressure increase together until about age 50
- DIASTOLIC PRESSURE DECREASES while SYSTOLIC PRESSURE CONTINUES the UPWARD trend
–> due to the aging process impairing cardiac fucntion, reducing diastolic pressure and altering vascular function causing the systolic pressure to INCREASE
describe the effects of longer term hypertension on the heart
- Hypertension leads to cardiac remodeling due to chronically elevated blood pressure resulting in VENTRICULAR HYPERTROPHY due to heart responding to HIGH AFTERLOAD
–> Hypertrophy increases risk for cardiovascular incidents (MI, HF and sudden cardiac death)
Describe the long term effects of hypertension on vasculature
- Vasculature remodeling occurs with high blood pressure
- Atherosclerosis = vascular remodeling and plaque formation
–> occurs through reactive process related to sheer stress on vessels along with hormonal factors
–> angiotension II mediates vascular remodeling
- INFLAMMATION
–> hypertension activates T-cell mediated response and further exacerbate end-organ damage
–> inflammation alters oxidative capacity in immune cells resulting in reactive oxygen stress (can influence vascular tone and protein expression)
describe the regulation of blood pressure (SHORT TERM)
- BAROREFLEXES
–> sense changes in blood pressure and send feedback to CNS to modulate sympathetic and parasympathetic outflow
–> modulate HR and Total peripheral resistance
- CHEMORECEPTORS
–> detect changes in chemical constituents of blood (oxygen, Carbon dioxide, and pH))
–> fall ina rterial oxygen saturation, increase in carbon dioxide saturation or decrease in pH STIMULATES a VASOCONSTRICTION and BRADYCARDIA
Describe ANGII role in long term regulation of BP
- Potent vasoactive substance
- DIRECT VASOCONSTRICTION and moderate sodium reabsorption
- Also stimulates ALDOSTERONE secretion from adrenal gland
aldosterone promotes even greater sodium reabsorption from kidney
describe the synthesis of ANGII
- Production of ANGII begings with release of angiotensinogen from liver
–> circulates in blood stream until it reaches the kidney
–> in the kidney, RENIN released from juxtaglomerular cells (response to sympathetic nerve stimulation) cleaves aniotensinogen into ANGI
–> ANGI circulates blood stream where it is futher cleaved into ANGII
Describe kidneys role in long term control of BP
- BLOOD VOLUME is a major factor in OVERAL ARTERIAL BLOOD PRESSURE (shifts blood volume vary directly with blood pressure through modulation of venous return)
- Under conditions of low arterial pressure, renal mechanisms CONSERVE WATER and SALT
- HIGH pressure, through an increase in resitance, will INCREASE SODIUM EXCRETION (water follows sodium –> called pressure-natriuresis) leading to REDUCTION in BLOOD VOLUME/pressure
- DYSFUNCTION in renal sodium/water handling WILL RESULT IN ABNORMAL BLOOD PRESSURES
describe the effect on aging in the vasculature
- in normal individuals, vessel wall easily accommodates pulsatile fluid flow due to lots of elastin in walls
- In older patients the vessel walls (aorta) become noncompliant
–> Vessel wall does not change with each ventricular ejection due to lots of collagen in wall
–> causes charp peaks of pusle pressure leading to differences transmitting downstream from aorta
describe the pathogenesis of essential hypertension
- CENTRAL FACTORS:
–> augemented symapthetic discharge
–> aberrant responses to peripheral signals
- VASCULAR DYSFUNCTION
–> exaggerated response to vasoconstrictors
–> depressed response to vasodilators
–> remodeling
- RENAL DYSFUNCTION = sodium and water handling defects
carotid sinus stimulation tx
- Used in resitant hypertension
- -> Is a pacemaker under the skin, gives stimulation to the carotid sinus to get an effect of dramatic decrease in blood pressure that is sustained over time.
- -> Uses the baroreflex to simulate a high blood pressure to use bodies normal technique at lowering blood pressure