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Medicine Cardiovascular > Blood Pressure > Flashcards

Blood Pressure Flashcards

1
Q

Blood pressure

A

The outward (hydrostatic pressure) exerted by blood pressure on the blood vessel walls

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2
Q

Systemic systolic arterial blood pressure

A

The pressure exerted by blood on the walls of the aorta and systemic arteries when the heart contracts. It should not reach or exceed 140mmHg under resting conditions

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3
Q

Systemic diastolic arterial blood pressure

A

The pressure exerted by blood on the walls of the aorta when the heart relaxes. Should not reach or exceed 90mHg under resting conditions

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4
Q

Hypertension

A

Clinical blood pressure of 140/90mmHg or higher and daytime average of 135/85mmHg

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5
Q

Pulse pressure

A

Difference between systolic and diastolic blood pressures. Should be between 30 and 50mmHg

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6
Q

What clinical items are used to determine blood pressure

A

Cuff sphygmomanometer and stethoscope

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7
Q

Korotkoff sounds (5)

A

1 - Peak systolic pressure
2/3 - Intermittent sounds are heard due to turbulent spurts of flow cyclically exceeding cuff pressure
4 - Minimum diastolic pressure, producing a muffled/muted sound
5 - No sound heard due to uninterrupted laminar flow

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8
Q

When are korotkoff sounds heard?

A

When cuff pressure is between 120-80mmHg

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9
Q

At which korotkoff sound is diastolic pressure measured?

A

5th korotkoff sound (when sound disappears)

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10
Q

Calculation for pressure gradient

A

Mean arterial pressure - central venous (right atrial) pressure

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11
Q

Mean arterial blood pressure

A

The average arterial blood pressure during a single cardiac cycle which involves contraction and relaxation of the heart

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12
Q

Calculations for mean arterial blood pressure (3)

A 
MAP = [(2x diastolic pressure) + systolic pressure]
MAP = diastolic blood pressure + 1/3 pulse pressure
MAP = cardiac output x systemic vascular resistance
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13
Q

Normal range for mean arterial blood pressure

A

70-105mmHg

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14
Q

Minimum mean arterial blood pressure required to perfuse vital organs

A

60mmHg

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15
Q

Why must mean arterial pressure be regulated within a narrow range? (2)

A
  • Pressure is high enough to perfuse internal organs including brain, heart and kidneys)
  • Pressure is not too high to ensure that there is no damage to blood vessels or extra strain placed on the heart
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16
Q

Cardiac output

A

Volume of blood pumped by each ventricle of the heart per minute

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17
Q

Cardiac output calculation

A

Stroke volume x heart rate

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18
Q

Stroke volume

A

Volume of pumped by each ventricle of the heart per heart beat

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19
Q

Systemic vascular resistance

A

Sum of the resistance of all the vasculature in the systemic circulation

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20
Q

Where is systemic vascular resistance greatest?

A

In the arterioles - major resistance vessels

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21
Q

Control centre for blood pressure

A

Medulla

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22
Q

Baroreceptors. Where are the following located and what are they innervated by?:

  • Carotid baroreceptors
  • Aortic baroreceptors
A
  • Carotid baroreceptors - located in the carotid sinus and are innervated by glossopharyngeal nerve (CN IX)
  • Aortic baroreceptors - located in the aorta and are innervated by the vagus nerve (CN X)
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23
Q

Postural hypotension

A

Results from failure of baroreceptor responses to gravitational shifts in blood when moving from horizontal to vertical position

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24
Q

Baroreceptor reflexes in the prevention of postural hypotension

A
  • Venous return decreases as an effect of gravity
  • MAP decreases
  • Rate of firing of baroreceptors thus reduced
  • Vagal tone to heart decreases and sympathetic tone increases, increases HR and SV
  • Sympathetic constrictor tone increases, increasing systemic vascular resistance
  • Sympathetic constrictor tone to veins increases, increasing venous return and stroke volume
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25
Q

Risk factors for postural hypotension

A 
Age
Medication
Certain diseases
Reduced intravascular volume
Prolonged bed rest
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26
Q

How is a positive result of postural hypotension determined?

A

By a drop, within 3 minutes of standing from lying position, in systolic blood pressure of at least 20mmHg without symptoms or a drop in diastolic blood pressure of 10mmHg with symptoms

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27
Q

What controls blood pressure changes in the short term?

A

Baroreceptor reflexes

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28
Q

Symptoms of postural hypotension

A

Dizziness, lightheadedness, blurred vision, faintness, falls

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29
Q

How much of the body fluid is intracellular fluid and how much is extracellular fluid?

A 
Intracellular = 2/3
Extracellular = 1/3
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30
Q

What is extracellular fluid volume?

A

Plamsa volume + interstitial fluid volume

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31
Q

Interstitial fluid

A

Fluid that bathes the cells and acts as the go-between the blood and body cells

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32
Q

What happens to control fluid levels if plasma volumes fall?

A

Compensatory mechanism shifts fluid from interstitial compartment to plasma compartment

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33
Q

2 main factors that influence extracellular fluid volume

A

Water excess or deficit

Sodium excess or deficit

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34
Q

Hormones which regulate extracellular fluid volume

A

Renin-angiotensin-aldosterone system
Natriuretic peptides
Antidiuretic hormone

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35
Q

Renin:

  • Where is it released from?
  • What does it do?
A
  • Granular cells in the juxtaglomerular apparatus in the kidneys
  • Stimulates the formation of angiotensin I in the blood from angiotensin produced in the liver
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36
Q

Angiotensin:

  • What converts angiotensin I to angiotensin II?
  • Functions of angiotensin II
A
  • Angiotensin converting enzyme
  • Stimulates the release of aldosterone from the adrenal cortex and causes systemic vasoconstriction, increasing SVR. Also stimulates thirst and ADH release and this contributes to increasing the plasma volume mainly brought about by aldosterone
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37
Q

What is angiotensin converting enzyme mainly produced by?

A

Pulmonary vascular endothelium

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38
Q

Aldosterone:

  • Which type of hormone is it?
  • Function
A
  • Steroid hormone
  • Acts on the kidneys to increase sodium and water retention thus increasing plasma volume and thus increasing blood pressure
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39
Q

What is the rate limiting step in RAAS system?

A

Renin secretion

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40
Q

What regulates the RAAS system?

A

Mechanisms which stimulate renin release i.e.:

  • Renal artery hypotension
  • Stimulation of renal sympathetic nerves
  • Decreased sodium concentration in renal tubular fluid
41
Q

What senses decreased sodium concentration in the renal tubular fluid?

A

Macula densa (specialised cells of kidney tubules)

42
Q

When are natriuretic peptides released?

A

In response to cardiac distension or neurohormonal stimuli

43
Q

What do natriuretic peptides do? (4)

A
  • Decrease renin release, decreasing blood pressure
  • Act as vasodilators, decreasing SVR and blood pressure
  • Cause excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure
  • Provide a counter-regulatory system for the RAAS system
44
Q

2 main types of natriuretic peptides released by the heart

A

Atrial natriuretic peptide (ANP)

Brain-type natriuretic peptide (BNP)

45
Q

Atrial natriuretic peptide:

  • How many amino acids in the peptide?
  • Where is it synthesised and stored?
  • What is it released in response to?
A
  • 28 amino acid peptide
  • Synthesised and stored by atrial muscle cells
  • Released in response to atrial distension (hypervolemic) states
46
Q

Brain-type natriuretic peptide:

  • How many amino acids in the peptide?
  • Where is it synthesised?
  • Where is it released from?
  • What is it released in response to?
A
  • 32 amino acid protein
  • Synthesised in heart (ventricles), brain and other organs
  • Released from ventricles
  • Released in response to stretching of ventricles caused by increased ventricular blood volume
47
Q

Steps in synthesis of brain-type natriuretic peptide

A

First synthesised as prepo-BNP which is cleaved to pro-BNP (108 amino acids )then finally BNP

48
Q

What BNP can be measured in patients with suspected heart failure?

A

Serum BNP and N-terminal piece of pro-BNP (76 amino acids)

49
Q

Another name for anti-diuretic hormone

A

Vasopressin

50
Q

Where is anti-diuretic hormone synthesised and stored?

A

Synthesised by hypothalamus and stored in the posterior pituitary

51
Q

What is secretion of anti-diuretic hormone stimulated by?

A

Reduced extracellular fluid volume or increased extracellular fluid osmolality [more water (main stimulus)]

52
Q

What does anti-diuretic hormone do? (2)

A

Acts in kidney tubules to increase reabsorption of water, increasing extracellular and plasma volume and hence cardiac output and blood pressure
Acts on blood vessels to cause vasoconstriction to increase SVR and blood pressure

53
Q

What does long term control of mean arterial blood pressure involve?

A

Control of blood volume by hormones

54
Q

What is hypertension a risk factor for? (6)

A

Cerebral haemorrhage, atheroma, renal failure, sudden cardiac death, cardiac failure, stroke

55
Q

Salt sensitive hypertension

A

Increase in dietary salt leads to increase in BP and so is controlled with reduced salt diet

56
Q

Secondary causes of hypertension (5)

A

Renal disease, endocrine disease, aortic disease, renal artery stenosis, drug therapy

57
Q

Renal causes of hypertension

A

Any renal disease, including renal artery stenosis, glomerulonephritis, chronic pyelonephritis, cystic diseases, interstitial nephritis

58
Q

How does renal disease lead to hypertension

A

Reduced renal blood flow → excess renin release → salt and water overload

59
Q

Endocrine causes of hypertension

A

Adrenal gland hyperfunction/tumours, Conn’s syndrome, Cushing’s syndrome, pheochromocytoma

60
Q

Conn’s syndrome

A

Excess aldosterone

61
Q

Cushing’s syndrome

A

Excess corticosteroid

62
Q

Pheochromocytoma

A

Tumour of the medulla resulting in excess noradrenaline

63
Q

What can benign hypertension eventually lead to?

A

Left ventricular hypertrophy, congestive heart failure, atheroma, increase aneurysm rupture, renal disease

64
Q

Diastolic blood pressure in malignant/accelerated hypertension

A

> 130-140

65
Q

What can malignant/accelerated hypertension lead to?

A

Cerebral oedema (seen as papilloedema), acute renal failure, acute cardiac failure, headache and cerebral haemorrhage

66
Q

Blood vessel findings in malignant/accelerated hypertension

A

Fibrinoid necrosis and endarteritis proliferans

67
Q

Endarteritis

A

Inflammation of the intima

68
Q

Hyaline arteriosclerosis

A

Thickening of the media and plasma proteins forced into the vessel wall. Results from hypertension causing microvascular injury

69
Q

How common is pregnancy related hypertension?

A

Extremely rare, common in up to 10% of pregnancies

70
Q

Primary hypertension

A

Hypertension that has no known secondary cause

71
Q

Stage 1 hypertension

A

A clinical blood pressure of 140/90mmHg or higher and a daytime average of 135/85mmHg or higher

72
Q

Stage 2 hypertension

A

A clinical blood pressure of 160/100mmHg or higher and a daytime average of 150/95mmHg or higher

73
Q

Severe hypertension

A

A clinical blood pressure of ≥180mmHg systolic and/or ≥110mmHg diastolic

74
Q

Ambulatory blood pressure monitoring:

  • When should readings be taken?
  • How many readings should be taken?
  • How is blood pressure calculated from these measurements?
A
  • At least 2 readings per hour during a person’s usual waking hours
  • At least 14 measurements
  • An average value of at least 14 measurements should be used to confirm the diagnosis
75
Q

Home blood pressure monitoring:

  • Describe the measurements
  • How is blood pressure determined from these measurements?
A
  • 2 consecutive seated measurements, at least 1 minute apart, twice daily for at least 4, but preferably 7, days
  • The measurements for the first day should be discarded and average value for the remaining values should be used
76
Q

White coat effect

A

When the blood pressure is high at clinic but normal/low at home

77
Q

Masked hypertension

A

When the blood pressure is normal/low at clinic but high at home

78
Q

What tests should be offered to everyone with hypertension?

A

Test urine for presence of protein, take blood to measure glucose, electrolytes, creatinine, cholesterol and estimated glomerular filtration rate, examine fundi for hypertensive retinopathy, 12-lead ECG

79
Q

Grade I hypertensive retinopathy

A

Slight or modest narrowing of the retinal arterioles with an arteriovenous ratio greater than or equal to 1:2

80
Q

Grade II hypertensive retinopathy

A

Modest to severe narrowing of retinal arterioles with an arteriovenous ratio less than 1:2 or arteriovenous nicking

81
Q

Grade III hypertensive retinopathy

A

Bilateral soft exudates or flame-shaped haemorrhages

82
Q

Grade IV hypertensive retinopathy

A

Bilateral optic nerve oedema

83
Q

ECG findings in left ventricular hypertrophy

A

ST depression, higher QRS complex

84
Q

Management for stage 1 hypertension

A

Offer lifestyle interventions, patient education and annual review of care to monitor blood pressure

85
Q

Management for stage 1 hypertension with either target organ damage or 10-year CV risk >20%, or stage 2 hypertension

A

Offer hypertensive treatment before original pathway

86
Q

Target blood pressure in patients <80 years old and ≥80 years old

A

<80 - 140/90mmHg or 135/85mmHg (home)

≥80 - 150/90mmHg or 145/84mmHg (home)

87
Q

Lifestyle interventions in the management of hypertension

A

Offer guidance about diet (reduce sodium and caffeine intake), weight reduction, exercise, alcohol consumption and smoking

88
Q

What can you provide to patients for patient education and adherence?

A

Information about benefits of drugs and side effects, details of patient organisations, an annual review of care

89
Q

First line medication for hypertensive patients <55 years old vs ≥55 years old or black patients at any age

A

<55 years old - ACE inhibitor/ARB

≥55 years old or black - calcium channel blockers or diuretic

90
Q

Second line medication for hypertensive patients

A

ACE inhibitor/ARB + calcium channel blocker
or
ACE inhibitor/ARB + diuretic

91
Q

Third line medication for hypertensive patients

A

ACE inhibitor/ARB + calcium channel blocker + diuretic

92
Q

Fourth line medication for hypertensive patients

A

ACE inhibitor/ARB + calcium channel blocker + diuretic +:

  • further diuretic therapy
  • alpha blocker
  • beta blocker
93
Q

What should ACE inhibitors/ARBs be replaced with in the management of hypertension of patients who are pregnant/fertile?

A

Beta blockers

94
Q

Why does combination therapy have fewer side effects than monotherapy?

A

You can block the side effects of one drug with another

95
Q

Causes of resistant hypertension

A

Non-concordance, white coat effect, pseudo-hypertension, lifestyle factors, drug interactions, secondary hypertension, true resistance

96
Q

When can patients be defined as having resistant hypertension?

A

When their BP remains uncontrolled on spironolactone

97
Q

Dose of spironolactone

A

12.5mg/day or 25mg every 2 days

98
Q

When to be cautious when using spironolactone

A

Diabetes and patients with low glomerular filtration rate

99
Q

New technology in lowering blood pressure

A

Renal denervation, baroreceptor stimulation, rox coupler

Medicine Cardiovascular (24 decks)

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