Hypertension Flashcards

1
Q

What factors combine to determine blood pressure?

A

Cardiac Output

Resistance to Bloodflow

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2
Q

What dictates the level of resistance to bloodflow?

A
  • The diameter of the lumen in the blood vessel
  • The viscosity of the blood
  • (also atherosclerosis obviously)
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3
Q

What is Cardiac Output?

A

Stroke Volume * Heart Rate

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4
Q

What is the normal range for cardiac output?

A

4 to 8 liters per minute

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5
Q

How is blood pressure measured?

A

What a sphygmomanometer; records systolic and diastolic pressure

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6
Q

What is the ideal blood pressure range? Systolic/Diastolic

A

90/60 to 120/80mmHg at rest

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7
Q

What is hypertension defined as in terms of blood pressure?

A
  • 140/90mmHg or higher at rest
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8
Q

Why is there an ideal blood pressure range?

A

Blood pressure needs to be high enough to allow the blood to reach all our organs and tissues at a sufficient rate, but not so high that it damages our blood vessels

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9
Q

How is blood pressure regulated in the short term?

A

Baroreceptors in the aortal arch and the carotid sinus detect pressure change, feeding back to the autonomic nervous system, which then either increases or reduces heart rate/cardaic contractility via sympathetic/parasympathetic fibres to increase or decrease blood pressure, respectively.

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10
Q

What system dictates long term regulation of blood pressure?

A

The Renin-Angiotensin System (RAAS) in the Kidney

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11
Q

Where is renin secreted from, and in response to what?

A

A peptide hormone released from the juxtaglomerular apparatus of the kidney in response to sympathetic stimulation, decreased kidney blood flow, and reduced sodium chloride delivery to the distal convoluted tubule. (All due to decreased blood pressure)

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12
Q

What is the role of Renin in the RAAS for long term blood pressure regulation?

A

Facilitates the conversion of angiotensinogen to angiotensin I.

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13
Q

What is ACE (Enzyme)?

A

Angiotensin converting enzyme:

  • Converts angiotensin I to active angiotensin II
  • Breaks down Bradykinin (potent vasodilator)
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14
Q

What is the role of Angiotensin II II in the RAAS system?

A

It causes vasoconstriction, increasing peripheral resistance, and causes aldosterone release, which increases sodium resorption and thus water retention, increasing blood volume and thus blood pressure

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15
Q

Where is Angiotensin 1 produced?

A

Liver

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16
Q

What is the mechanism when too high blood pressure is detected?

A

There isn’t one, other than reducing renin secretion

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17
Q

What do the systolic and diastolic values mean for blood pressure?

A

Systolic is highest it will get (during contraction) and Diastolic is lowest it will get (between contraction)

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18
Q

Why is Mean Arterial Pressure a potentially better metric than looking at Systolic or Diastolic blood pressure?

A

You can be high in one and not the other, so you may have undetected hypertension if you only use the Sys/Dias metric because you wont fit the measure of hypertension

19
Q

How is Mean Arterial Pressure calculated?

A

MAP = DP + 1/3SP

20
Q

How is hypertension influenced by age?

A

Older you are the higher the prevalence

21
Q

What are the two main types of hypertension?

A

Primary/Essential Hypertension

Secondary Hypertension

22
Q

What is Primary/Essential/Idiopathic hypertension?

A

No known cause, about 9% of cases are this

23
Q

What is secondary hypertension?

A

The product of something else like kidney disease, diet, hormonal imbalance, obesity, etc.

24
Q

What are the risk factors for hypertension?

A
  • Genetic predisposition
  • Excessive sodium intake
  • Obesity
  • Sedentary lifestyle
  • Stress
  • Excessive Alcohol Consumption
  • Age
  • Oral Contraceptive
25
Q

What is natriuresis?

A

Excretion of sodium in the urine

26
Q

What is the Guyton Hypothesis?

A

Sustained hypertension can occur only when the relationship between arterial pressure and natriuresis is abnormal

27
Q

How does obesity impact hypertension?

A
  • Increased cardiac output
  • Increased sympathetic renal nerve traffic increasing sodium retention, due to high leptin
  • Increased RAAS activation due to increased adipose tissue secretion of angiotensinogen
  • Hyperinsulinemia. Insulin also causes sodium resorption
28
Q

what is the prevalence of hypertension in the UK?

A
  • 10% of adult population recieving treatment for hypertension
  • Approx 15% of adults have untreated hypertension
29
Q

How does chronic stress increase risk of hypertension?

A

-Frequently or constantly increased secretion of catecholamines (like adrenaline and cortisol) lead to increased HR, Cardiac Output and Blood Pressure.

30
Q

How does excessive alcohol consumption lead to hypertension?

A

Alcohol consumption acutely raises blood pressure, and excessive habitual alcohol intake chronically raises blood pressure, but the mechanisms are unclear.

31
Q

what is Double Product?

A

A value used to describe the amount of work the heart is having to do, calculated by:

HR * Systolic BP

32
Q

What physiological changes occur to the heart in response to chronic hypertension?

A

Cardiac Hypertrophy/Pronounced thickening of the cardiac walls but with no change in chamber size

33
Q

What occurs to blood vessels in chronic hypertension?

A

Excessive shear and direct stress, making damage more likely, which provides more gaps for LDL to fit under, to cause atherosclerosis

34
Q

Apart from CHD, what else does hypertension increase the risk of?

A

Stroke and Intermittent Claudication

35
Q

What are the most common pharmacological treatments for blood pressure?

A
  • Beta Blockers
  • Alpha Blockers
  • Calcium Channel Blockers
  • Diuretics
  • ACE Inhibitors
  • Angiotensin II Receptor Blockers
36
Q

How do Beta Blockers work? (Beta-Adrenergic Blocking Agents)

A

Reduces Heart rate by blocking the effects of adrenaline/epinephrine

37
Q

How do Alpha Blockers work? (Alpha-Adrenergic Blocking Agents)

A

Reduces vascular tone/vasoconstriction by blocking the effects of noradrenaline/norepinephrine

38
Q

What are the most common non-pharmacological treatments of hypertension?

A
  • Diet (Weight loss and controlled salt intake)
  • Relaxation/Stress Reduction
  • Exercise
39
Q

How does training status impact the relationship between menopause and blood pressure?

A

-Blood pressure did not change pre-post menopause for trained women, but it increased in sedentary women

40
Q

How does regular exercise chronically reduce blood pressure?

A

Unclear, but proposed:

  • Increased lumen size
  • Decreased adiposity and body mass (indirect)
  • Increased Insulin sensitivity
  • Decreased Stress
  • Decreased Arterial Stiffness
41
Q

How does exercise acutely reduce blood pressure?

A
  • Reduced norepinephrine

- Reduced sympathetic activity leading to reduced angiotensin II

42
Q

What evidence exists to suggest an optimal exercise intensity for lowering blood pressure?

A

Hagberd et al 1989 found that 50% VO2max exercise was superior to 70% VO2max for reducing blood pressure. Otherwise the best intensity is not clear.

43
Q

What impact does existing blood pressure have on the impact of exercise on blood pressure? Give evidence

A

Cornelissen and Fagard found that exercise reduced blood pressure in hypertensive individuals more than normotensive individuals, but the decrease was found in both.

44
Q

What impact does isometric exercise have on blood pressure? Give evidence

A

Smart et al 2019 found consistent effective response of isometric exercise on decreasing blood pressure