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NURS 1650 - Here We Go Again > Pathophysiology of Hypertension > Flashcards

Pathophysiology of Hypertension Flashcards

1
Q

What is systolic blood pressure?

A

The highest level of pressure right after the ventricles contract

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2
Q

What is diastolic blood pressure?

A

The lowest level of pressure right before the next contraction of the ventricles

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3
Q

What is stroke volume (SV)?

A

The amount of blood ejected from the ventricle with each contraction

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4
Q

What is systemic vascular resistance (SVR)?

A

The resistance to blood flow offered by all of the systemic vasculature

AKA total peripheral resistance (TPR)

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5
Q

Vasoconstriction does what to SVR?

A

Vasoconstriction causes SVR to increase

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6
Q

Vasodilation does what to SVR?

A

Vasodilation causes SVR to decrease

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7
Q

What role does the autonomic nervous system have in regulating heart rate?

A

Parasympathetic System (vagus nerve, acetylcholine)

  • Slows the heart
  • Acetylcholine acts as muscarinic receptors
  • Resting state controlled by the vagus nerve
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8
Q

What role does the sympathetic nervous system have on regulating heart rate?

A

“Fight or Flight”

Speeds up the heart

Norepinephrine acts at Beta 1 adrenergic receptors

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9
Q

What are the 3 determinants of stroke volume?

A

Preload

Afterload

Contractility

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10
Q

What is preload?

A

The amount of blood filling the heart right before it starts to contract (same as EDV)

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11
Q

How does volume affect preload?

A

A decrease in volume results in a decrease in preload

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12
Q

What role does the SNS have on preload?

A

SNS causes either venoconstriction or venodilation

Venoconstriction results in an increase in preload (bc there is more blood being squeezed toward the heart)

Venodilation results in a decrease of preload

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13
Q

Relaxation of the ventricle normally during diastole imfluences:

A

Preload

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14
Q

Filling time of the ventricle controls preload by:

A

Determining the length of diastole

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15
Q

Why is the venous system important to keep in mind when thinking about preload?

A

Increased venous return to the heart will increase preload

An increase of blood volume then also increases venous return to the heart

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16
Q

How does preload affect stroke volume? Describe how it does this

A

Increase in preload results in an increase in stroke volume

An increase in preload results in an increase stretch of cardiac sarcomeres

A stronger contraction is made which increases stroke volume

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17
Q

What does the Frank-Starling Mechanism describe?

A

A healthy heart automatically adjusts its output (SV) to match the EDV / Preload

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18
Q

What is afterload?

A

The pressure the ventricle sees after it starts to contract

“the force needed to be overcome to pump the blood out”

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19
Q

Afterload is determined by what two things?

A

Systemic vascular resistance

Valve integrity

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20
Q

How does systemic vascular resistance affect afterload?

A

Increase in SVR will increase afterload

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21
Q

How does valve integrity affect afterload?

A

A stiffened valve/one that does not fully open will increase afterload, making it more difficult for blood to pass through

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22
Q

How does afterload affect stroke volume? Why?

A

An increase in afterload causes a decrease in stroke volume

More pressure needed to be overcome will result in less blood being pumped out

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23
Q

What is contractility?

A

The intrinsic strength of cardiac contraction

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24
Q

How does the SNS affect contractility?

A

Activation of Beta 1 receptors results in an increase in contractility

25
Q

How does contractility affect stroke volume?

A

An increase in contractility results in an increase in stroke volume

A decrease in contractility results in a decrease in stroke volume

26
Q

What things determine SVR?

A

Vessel radius

Length and blood viscosity

27
Q

Resistance is _____ proportional to the radius to the 4th power. What does this mean?

A

Inversely proportional

This means that as radius decreases, resistance increases

28
Q

Blood flow is ____ proportional to the radius to the 4th power. What does this mean?

A

Directly proportional

When the radius decreases, blood flow decreases

29
Q

How does the SNS prevent orthostatic hypotension?

A

When we go from a supine to a standing position, alpha-1 adrenergic receptors are activated

They cause vasoconstriction

30
Q

How do voltage-gated calcium channels on smooth muscle affect SVR?

A

When activated/opened, they cause an increase in calcium inflow and cause vasconstriction

31
Q

What receptors make good targets for the pharmacotherapy of hypertension?

A

Beta 1

Alpha 1

Calcium Channels

32
Q

Why are arterioles the major blood vessel type that influences SVR?

A

They provide 2/3 of the resistance to flow in the systemic circulation

Their strong muscular walls allow the internal diameters to increase or decrease tremendously

Small changes in the radius of the arteriolar lumen have large effects on blood pressure

33
Q

What hormones and local mediators cause constriction/increase in SR/increase in BP? How do they do this?

A

Angiotensin II

Aldosterone: conserve sodium and blood volume

Vasopressin/ADH: act on kidneys to preserve water and blood volume; act on vascular smooth muscle to cause vasoconstriction

Endothelin: acts locally to constrict blood vessels

Norepinephrine, epinephrine: activate alpha-1 adrenergic receptors in vascular smooth muscle

34
Q

Which hormones and local mediators result in dilation/decrease in SVR/decrease in BP? How do they do this?

A

Nitric Oxide: act locally to dilate/relax blood vessels

ANP, BNP: get rid of salt and decrease blood volume; acts on vascular smooth muscle to cause vasodilation

Epinephrine on B2 receptors in certain vascular beds

Presynaptic alpha-2 adrenergic receptors: prevent further release of norepinephrine

35
Q

What do baroreceptors do?

A

They are mechanoreceptors that respond to changes in stretch/tension of arterial walls

Primarily found in the arch of the aorta and carotid artery

Monitor MAP variations on a moment-by-moment basis

36
Q

What is a baroreceptor reflex?

A

Changes initiated by baroreceptors

37
Q

Describe the process in which baroreceptors cause a rise in BP

A

Decrease in MAP

Decrease in blood vessel wall stretch

Baroreceptors sense this decrease in stretch

38
Q

Describe the process in which baroreceptors cause a rise in BP

A

Decrease in MAP

Decrease in blood vessel wall stretch

Baroreceptors sense this decrease in stretch
——

Decrease in APs

Increased SNS activity

Activation of alpha-1 in smooth muscle (increase in SVR)

Beta-1 receptors in the heart (increase HR and CO)

Decreased vagal activity (increase HR and CO)

OVERALL: rise in BP

39
Q

How does the baroreceptor reflex apply to patients in bed?

A

Important mechanism when changing positions

The reflex can become downregulated even after a short hospital stay

Keep in mind when getting patients out of bed for the fist time

40
Q

How does chronic hypertension affect baroreceptors?

A

The baroreceptors adapt and become less sensitive

They are best suited to respond to sudden, acute changes in BP

41
Q

What is elevated BP?

A

120/80 - 139/89

42
Q

What is essential hypertension?

A

Hypertension common and correlated with prevalence of obesity and a diet high in fats and sodium/low in fruits and vegetables

We cannot pinpoint a cause of their HTN

43
Q

What is white coat hypertension?

A

HTN in the healthcare setting that is higher than the person’s actual normal, day-today BP

44
Q

Dysfunction in what organs/systems contribute to HTN?

A

Kidneys (effect on blood volume, Na + H2O movement)

CNS (SNS signaling)

Vasculature (Contraction, relaxation)

45
Q

What are some potentially treatable causes of hypertension?

A

CKD

Renovascular (renal artery stenosis)

Endocrine (aldosterone excess, pheochromocytoma tumor on adrenal gland producing epinephrine, cortisol excess)

Preeclampsia

46
Q

How must we assess hypotension? What should we look at?

A

In general, it is <90/60

Is the person symptomatic? (dizzy, falls)

Is it due to a drop in BP, or is this their baseline BP?

Potential infectious process occurring? (sepsis)

Is the BP falling? (like how we see in shock)

47
Q

Why is kidney disease a major risk factor for hypertension?

A

The kidneys control blood volume, H2O and Na excretion

48
Q

What are the clinical manifestations of HTN?

A

May be asymptomatic for many years (“the silent killer”)

Nonspecific headaches

End organ damage with untreated HTM

49
Q

What are the major organ systems affected by uncontrolled HTN?

A

Heart and arteries

Kidneys

Brain

Eyes

Reproductive system

50
Q

What effect does HTN have on blood vessels?

A

It enhances atherosclerosis

51
Q

What is the difference between arteriosclerosis and atherosclerosis?

A

Arteriosclerosis:
- Umbrella term
- Often age-related
- General increased collagen disposition –> increased stiffness and decreased elastic recoil of vessels

Atherosclerosis:
- Specific type of arteriosclerosis
- Due to cholesterol
- Seen in younger ages

52
Q

Hypertrophy occurs in HTN because:

A

Cardiac stress overworks the heart

More work is needed to pump blood out

Makes the cells grow bigger

53
Q

How does uncontrolled HTN do to afterload as the heart pumps blood into the aorta?

A

Increases afterload

54
Q

If the left ventricle hypertrophies and the walls of the ventricle get bigger and bigger, what will it do to the size of the ventricular chamber (the space inside the ventricle)?

A

It will become smaller

Less room for blood

55
Q

Will a hypertrophied muscle be able to relax as well as a normal ventricle?

A

No

56
Q

What will happen to stroke volume in a hypertrophied ventricle? Why?

A

Decrease in SV

There is less possible volume in the chamber

There is a decreased ability to refill

57
Q

What overall effect does HTN have on the renal arterioles?

A

Hypertrophy and constriciton

58
Q

What overall effect does HTN have on the brain?

A

Hemorrhage, stroke

59
Q

What overall effect does HTN have on the eyes?

A

Retinopathy

Retinal detachment

NURS 1650 - Here We Go Again (20 decks)

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