week 4- hypertension Flashcards

(32 cards)

1
Q

hypertension

A
  • 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)
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2
Q

prevalence of HT

A
  • 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
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3
Q

isolated systolic hypertension

A
  • average SBP greater than or equal to 140 mmHg coupled with an average DBP less than 90 mm Hg
  • more common in older
    adults
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4
Q

stage 1 HT

A

130-139/80-89 mmHg

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5
Q

stage 2 HT

A

140/90 mmHg<

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6
Q

factors contributing to blood pressure

A

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

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7
Q

cardiac output

A

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

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8
Q

factors that influence CO

A

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

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9
Q

peripheral vascular resistence

A
  • force opposing the movement of blood
    within the blood vessels
  • when BV constrict, PVR increases
  • when BV dilate, PVR decreases
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10
Q

alpha 1 receptors

A

primarily found on vascular smooth muscle and are responsible for vasoconstriction when stimulated by catecholamines like norepinephrin

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11
Q

alpha 2 receptors

A
  • located in the brain and periphery
  • modulate sympathetic outflow, potentially lowering blood pressure through mechanisms like reduced neurotransmitter release
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12
Q

beta 1 receptors

A
  • mainly located in the heart (and kidneys), increase heart rate and contractility when stimulated
  • stimulation in the kidneys can lead to renin release
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13
Q

beta 2 receptors

A

found in blood vessels and other organs, cause vasodilation when activated

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13
Q
A
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14
Q

dopamine

A
  • 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
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15
Q

baroreceptors

A
  • 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
16
Q

SNS

A

activation increases heart rate (HR) and
cardiac contractility, produces widespread vasoconstriction in the peripheral arterioles and promotes the release of renin from the kidneys

17
Q

vascular endothelium

A
  • 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
18
Q

how does RAAS increase BP?

A
  • 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)
19
Q

how does the endocrine system regulate BP?

A
  • 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
20
Q

etiology of HT

A

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

21
Q

causes of primary HT

A
  • 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
22
Q

clinical signs of secondary hypertension

A
  • unprovoked hypokalemia
  • abdominal bruit
  • variable pressures with history of tachycardia, sweating, and tremor
  • family history of renal disease
23
Q

causes of secondary HT

A
  • 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
24
25
symptoms of HT
- fatigue, reduced activity tolerance, dizziness, palpitations, angina, and dyspnea - sudden, severe headache can indicate a hypertensive crisis
26
diagnostic tests of HT
a) lipid panel, metabolic panel and thyroid panel b) urinalysis:to check for protein in the urine (albumin-to-creatinine ratio) and hematuria (blood in the urine) c) ECG: assess heart rhythm and identify any signs of heart damage due to hypertension d) physical exam including eye exam, CV exam and abdominal exam
27
ambulatory blood pressure monitoring
- monitoring takes dozens of readings over a continuous period - also calculates changes in BP and heart rate, BP distribution pattern - can be used to confirm a diagnosis of HT
28
pharmacological management of HT
a) thiazide diuretics: encourage excretion of Na and water b) CCBs: relax BV by preventing calcium from entering the heart and blood vessel muscles c) ace inhibitors/ARBs: block the production of a hormone that narrows BV d) beta blocker e) renin inhibitors
29
orthostatic hypotension
defined as a decrease of 20 mm Hg or more in SBP, a decrease of 10 mm Hg or more in DBP
30
hypertensive crisis
- a severe and abrupt elevation in BP, arbitrarily defined as a DBP above 120 to 130 mm Hg - evidence of acute organ damage - requires immediate hospitalization and administration of IV antihypertenisive drugs | 180/120 mmHg <
31
hypertensive urgency
- elevated blood pressure without acute organ damage, usually managed with oral medications and close follow-up - develops over days or weeks