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NUR 201 Week 5 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Review of the Circulatory System

  • Right side of the heart pumps deoxygenated blood to the lungs to pick up oxygen and the oxygenated blood is returned to the left side of the heart where it is pumped away from the heart all the way through arteries, arterioles, and capillary bed
  • In the capillary bed there’s gas exchange
  • Once gases have been exchanged, there’s a return flow to the heart through the capillary bed, the venules, and veins
A
  • Largest veins are superior and inferior vena cavas
  • Largest artery is the aorta
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2
Q

?

Is the force of blood pushing against the artery walls as it flows through them (arterial pressure [AP])

A

Blood pressure

  • High pressure over time may cause inflammation, fatty accumulation, & atherosclerosis
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3
Q

AP = CO x PVR

AP = Arterial Pressure

CO = Cardiac Output

PVR = Peripheral Vascular Resistance

A

CO = Heart Rate (HR) x Stroke Volume (SV)

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4
Q

?

Is the volume of blood expelled from the ventricles w/each beat (SV) multiplied by bpm (HR)

A

CO

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5
Q

?

Is the resistance to the flow of blood determined by the tone of the vascular musculature, the diameter of blood vessels; whether they are dilated or constricted will effect BP

A

PVR

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6
Q

An increase in CO or PVR will increase BP

CO = ? x ?

Heart rate, contractility

Blood volume
Venous blood return to heart

PVR
> Arterial constriction

A

HR x Stroke Volume

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7
Q

Mean arterial pressure (MAP)

MAP = DP + 1/3 (SP - DP)

  • A minimum MAP of ___ mmHg is required to perfuse vital organs
A

60

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8
Q

Autoregulation of BP - Compensatory mechanisms to maintain homeostasis

  1. Sympathetic baroreceptors
  2. Regulation of fluid volume
  3. Renin-Angiotensin System, aldosterone
  4. Vascular autoregulation
A
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9
Q
  1. ?

Are pressure-sensitive nerve endings located in the aorta, left ventricle, and carotid sinus

Slow HR and dilate vessels when BP elevated; increase HR and constrict blood vessels when BP is low

A

Baroreceptors

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10
Q

__ receptors in blood vessels cause vasoconstriction - increases PR

A

Alpha

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11
Q

__ receptors in heart stimulate increase in HR - increase in CO

A

Beta

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12
Q

Beta

Respond to ___ (increase HR and decrease bronchospasm) and beta blockers (decrease HR)
> Increases rate and force of heart
> Relaxation of bronchial muscles

A

epinephrine

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13
Q

Alpha

Responds to ___

Causes increased PVR, dilation of pupils, contraction of pilomotor muscles (goose bumps)

A

norepinephrine

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14
Q
  1. Regulation of Fluid Volume

Excess sodium or water increases CO & BP

Kidneys will diurese the extra volume and sodium

A

If BP dropping, kidneys will reabsorb sodium and water to increase BP

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15
Q
  1. Renin-Angiotensin System

A) Decreased blood volume - the body senses a decreased BP

A
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16
Q

B) Decreased blood flow to kidney increases the release of renin from kidney which increases angiotensin I that’s released and converts to angiotensin II;

This increases renal and systemic blood vessel constriction, so blood vessel constriction will increase blood flow

A
  • Two-fold, angiotensin II stimulates the release of aldosterone from the kidney which increases sodium and water retention (has to do with volume & increases BP as well)
17
Q
  1. Vascular Autoregulation
  • Intrinsic vessel dilation/constriction locally at certain organs (brain, heart, kidneys)
  • Is a manifestation of local blood flow regulation
A
  • Defined as the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure
  • For example, if perfusion pressure is decreased to an organ (e.g., by partially occluding the arterial supply to the organ), blood flow initially falls, then returns towards normal levels over the next few min
  • This autoregulatory response occurs in the absence of neural and hormonal influences and therefore is intrinsic to the organ
18
Q

Categories of BP in Adults

A

It’s important to modify risk factors by implementing lifestyle changes prior to the individual becoming hypertensive and requiring implementation of rx’s

Treatment starts w/identification of risk factors and modifying them to optimize BP and decrease risk of long-term complications

19
Q

Primary or essential HTN accounts for 90% of people w/HTN

Not caused by an existing health problem

A

Secondary HTN develops r/t another disease process

20
Q

Primary or secondary HTN?

  • Kidney disease / primary aldosteronism
  • Pheochromocytoma / Cushing disease
  • Coarctation of the aorta / brain tumors
  • Encephalitis / Pregnancy
  • Drugs/hormones: estrogen, glucocorticoids, mineralocorticoids, sympathomimetics
A

Secondary

21
Q

Primary or secondary HTN?

  • Fhx / African-American ethnicity
  • Hyperlipidemia / smoking
  • > 60 yrs age or post menopausal / excess caffeine, sodium, ETOH
  • Overweight, obesity / sedentary lifestyle
  • Low potassium, calcium, magnesium
A

Primary (essential)

22
Q

Complications of Chronic HTN

  • Blood vessel damage - atherosclerosis, PVD
  • Coronary artery disease - MI
  • Enlarged heart - CHF
  • Cerebrovascular disease - CVA
  • Kidney failure - dialysis/transplant
  • Eyes - retinal hemorrhage/blindness
A

Target organ damage

  • Sheering forces from the increased BP damage the intimal layers of the blood vessels causing edema & fibrin, fatty plaque accumulation followed by atherosclerosis
  • Small vessels become narrow & blood flow lessens to particular “target” organs
  • Vessels become less flexible and can occlude
    > Heart, brain, eyes, kidneys; intermittent claudication of LE’s
23
Q

Nursing Assessment

Complete history
- Social/habits
- Rx’s
- Sx’s (target organ involvement?)

A

Physical assessment
- CV assessment
- Lung sounds
- MS/neuro
- Vision, renal

24
Q

Diagnostics

  • Risk factor assessments - implement lifestyle modifications (i.e., smoking cessation)
  • Urinalysis
  • Inc albumin in the urine & GFR will decrease if there’s an issue w/the kidneys
  • Blood chemistry
  • Cholesterol, LDL/HDL, triglycerides
  • Electrolytes (K+, Na+, Mg2+)
  • Blood sugars
  • CRP is released in acute inflammatory conditions & w/necrosis
  • Homocysteine (an amino acid) increases risk of collagen & cardiovascular disorders
A
  • 12-lead ECG
  • Prior MI or cardiomegaly?
  • Echo
  • Would look at signs of cardiomegaly & CHF
  • Fundoscopic exam
  • Looks at the back of the eye to check for any leaking capillaries or other identifiable dyscrasias in the eye
25
Q

Lifestyle modifications based on modifiable risk factors (Healthy People 2030)

  • Smoke cessation
  • Weight reduction w/exercise - static isometric, aerobic, & resistance training
  • Restricted caloric intake - DASH diet
    > Omega-3 fatty acids (fish/plant sources: salmon, canola oil, mackerel, walnuts & walnut oil, herring, soybean & soybean oil, tuna, flaxseed ground & oil, rainbow trout, wheat germ & oat germ, sardines, green leafy vegetables)
    > Omega-3’s may reduce the risk of clots that may cause an MI & possible sudden death
A
  • Low fat/cholesterol diet & omit trans-fatty acids
  • Sodium limited to 1500 mg/day
    > Increase Mg2+, Ca2+, & K+ & reduce intake of saturated fat & total fat
  • Limit ETOH & stress
  • Monitor and treat comorbidities: diabetes, dyslipidemia
26
Q

Cholesterol Diet & Medications

  • Total cholesterol
  • HDL (good)
  • LDL (bad)
  • Triglycerides
  • Saturated & trans-fatty acids
A
27
Q

?

Are serum lipids that include HDL and LDL

A

Cholesterol

28
Q

?

“Bad”

Part of the total cholesterol value that should be <130 mg/dL; contributes to fatty build-up in the arteries (atherosclerosis)
> This narrows the arteries & increases the risk for MI, CVA, & PAD

A

LDL

29
Q

?

Are the most common type of fat in the body; store excess energy from the diet

A high level combined w/high LDL or low HDL is linked w/fatty buildups within artery walls, which increases risk of MI & CVA

A

Triglycerides

30
Q

?

Part of the total cholesterol value that should be more than >45 mg/dL for men & >55 mg/dL for women

Carries “bad” cholesterol away from the arteries & back to the liver, where LDL is broken down and passed from the body

A

HDL

  • Only 1/3 to 1/4 of of blood cholesterol is carried by HDL
31
Q

Sodium Stowaways

  • Snacks
  • Seasonings & non-nutritive sweeteners (MSG, sodium saccharine)
  • Soups, sauces
  • Smoked meats & fish
  • Sauerkraut & other pickled foods
  • Sodium-processed luncheon meats
A

Anti-hypertensives

  • Diuretics
  • Beta-adrenergic blockers
  • Ace inhibitors
  • Angiotensin II receptor blockers
  • Calcium channel blockers
32
Q

?

Decrease volume by working on the kidneys

K+ sparing concern w/elevated K+ levels systemically; decrease K+ intake - spironolactone

Loop (__) and thiazide (__) excrete K+ and Mg+
> Concern w/low circulating Na, K, & Mg levels

Add PO intake of these electrolytes; may cause gout exacerbation; glucose regulation may be altered

A

Diuretics

furosemide; hydrochlorothiazide

33
Q

?

i.e., metoprolol, atenolol

Alpha-1 receptors on blood vessels, beta-1 receptors on heart; beta-2 receptors in lungs (bronchospasm)
- When alpha-1 receptors are blocked, blood vessels dilate, dropping pressure. Beta-1 receptors on the heart drop HR

  • Depression, fatigue, sexual dysfunction
  • May affect glucose production & hypoglycemic manifestations may be altered
A

Beta-adrenergic blockers - “LOL”

34
Q

?

i.e., lisinopril, captopril

Vasodilate & act on aldosterone (which will normally absorb Na & water)
> Person excretes more Na+ & water, decreasing the volume and vasodilates blood vessels

  • S/S: decreased K+ excretion, causing possible hyperkalemia & cough
  • Take precautions w/orthostatic hypotension
A

Ace inhibitors - “pril”

35
Q

?

Block the release of aldosterone & block angiotensin II from the angiotensin I receptors
> Cause vasodilation & decrease PVR

i.e., losartan, valsartan

  • May cause hyperkalemia - avoid foods w/high K+
A

Angiotensin II receptor antagonists (ARBs)

36
Q

?

Slows HR @ SA & AV node, vasodilates vessels

i.e., verapamil, amlodipine, diltiazem

! Avoid grapefruit juice w/these as may cause organ dysfunction

A

Calcium channel blockers

37
Q

Hypertensive Crisis: BP ?

  • Semi-fowler position (decrease ICP)
  • Oxygen
  • IV anti-hypertensives slowly to prevent ischemia to brain, heart, & kidneys
    > IV labetalol, nicardipine, nitroprusside, or fenoldopam
    ! Reduce SBP by no more than 25% in 1st hr of treatment
  • Monitor BP
  • Observe for complications
A

> 180/120

38
Q
  • Severe headache
  • Dizziness
  • Blurred vision
  • SOB
  • Epistaxis
  • Severe anxiety
A

Complications

  • Neurologic or cardiovascular like seizures, numbness, weakness or tingling of extremities
  • Dysrhythmias or chest pain (possible indicators of target organ damage)

NUR 201 Week 5 (5 decks)

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