week 4- hypertension Flashcards
(32 cards)
hypertension
- sustained elevation of systemic arterial blood pressure (BP) and is the leading cause for visits to primary care physicians
- high BP is the most significant modifiable risk factor for cardiovascular disease and mortality in canada
- 140/90 mmHg< (180/120 is considered a HT crisis)
prevalence of HT
- increases with age
- women with high BP have a greater risk for CVD
- indigenous people have a higher incidence of CVD than non-indigenous people in canada
- more prevalent in older women than in older men
isolated systolic hypertension
- average SBP greater than or equal to 140 mmHg coupled with an average DBP less than 90 mm Hg
- more common in older
adults
stage 1 HT
130-139/80-89 mmHg
stage 2 HT
140/90 mmHg<
factors contributing to blood pressure
a) cardiac output: inc CO, inc bp
b) peripheral vascular resistance: inc PVR, inc bp
c) volume of circulating blood: inc vol, inc bp
d) viscosity of blood: inc viscosity, inc bp
e) elasticity of vessels walls: dec elasticity, inc bp
cardiac output
the volume of blood ejected from the heart per minute
CO in L/min = stroke volume (SV) x HR
SV = the amount of blood pumped out of the left ventricle per beat
factors that influence CO
a) increase in CO: sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels
b) decrease in CO: include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis
peripheral vascular resistence
- force opposing the movement of blood
within the blood vessels - when BV constrict, PVR increases
- when BV dilate, PVR decreases
alpha 1 receptors
primarily found on vascular smooth muscle and are responsible for vasoconstriction when stimulated by catecholamines like norepinephrin
alpha 2 receptors
- located in the brain and periphery
- modulate sympathetic outflow, potentially lowering blood pressure through mechanisms like reduced neurotransmitter release
beta 1 receptors
- mainly located in the heart (and kidneys), increase heart rate and contractility when stimulated
- stimulation in the kidneys can lead to renin release
beta 2 receptors
found in blood vessels and other organs, cause vasodilation when activated
dopamine
- peripheral vasostimulant used to treat low blood pressure, low heart rate, and cardiac arrest
- intermediate infusion rates (from 2 to 10 micrograms/kg/min) stimulate myocardial contractility and increase electrical conductivity in the heart leading to increased cardiac output
baroreceptors
- specialized nerve cells located in the carotid artery and the arch of the aorta, sense changes in BP
- when BP is increased, these receptors send inhibitory impulses to the sympathetic vasomotor centre in the brainstem resulting in decreased HR, decreased force of contraction, and vasodilation in peripheral
arterioles
SNS
activation increases heart rate (HR) and
cardiac contractility, produces widespread vasoconstriction in the peripheral arterioles and promotes the release of renin from the kidneys
vascular endothelium
- the endothelium produces and releases a variety of molecules that affect blood vessel tone
- NO relaxes blood vessels and lowers blood pressure
- endothelin-1 constricts blood vessels and raises blood pressure
how does RAAS increase BP?
- kidneys secrete renin, which initiates the RAAS cascade
- leads to the production of angiotensin II, which constricts blood vessels and increases blood pressure
- aldosterone is also released, which helps the kidneys retain sodium and water, further raising blood pressure
- kidneys also play a role inpressure natriuresis,the process of increasing sodium and water excretion when blood pressure rises (helps lower blood volume and blood pressure)
how does the endocrine system regulate BP?
- adrenal medulla releases epinephrine in response to SNS stimulation.
- epinephrine activates β2-adrenergic receptors, causing vasodilation
- adrenal cortex is stimulated by angiotensin 2 to release aldosterone
- aldosterone stimulates the kidneys to retain sodium and water, increasing BP
- ADH is released from the posterior pituitary gland in response to an increased blood sodium and osmolarity level
- this promotes the reabsorption of water in the distal and collecting tubules of the
kidneys, resulting in an increase in blood volume and BP
etiology of HT
a) primary hypertension: elevated BP without an identified cause
- accounts for 90% to 95% of all cases of HTN
b) secondary hypertension: elevated BP with a specific cause that often can be identified and corrected
- accounts for 5% to 10% of HTN in adults, and more
than 80% of HTN in children
causes of primary HT
- family history, ethnicity
- high sodium, low potassium intake
- diabetes mellitus or insulin resistance
- obesity
- excessive alcohol intake
- stress and inc SNS activity
- endothelial cell dysfunction (excess vasconstriction)
- altered RAAS system
clinical signs of secondary hypertension
- unprovoked hypokalemia
- abdominal bruit
- variable pressures with history of tachycardia, sweating, and tremor
- family history of renal disease
causes of secondary HT
- coarctation or congenital narrowing of the aorta
- renal disease such as renal artery stenosis and parenchymal disease
- endocrine disorders such as pheochromocytoma, Cushing’s syndrome, and hyperaldosteronism
- neurological disorders such as brain tumours, quadriplegia, and head injury
- sleep apnea
- medications
- pregnancy-induced hypertension