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Cardiovascular System > Control Of Bood Pressure & Hypertension > Flashcards

Control Of Bood Pressure & Hypertension Flashcards

1
Q

What is the function of the arterial baroreceptor reflex? Where are the sensing sites?

A

Detect the mean arterial pressure

Sensing sites in aortic arch and carotid sinus

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2
Q

What kind of sensing site receptors are in the aortic arch and carotid sinus?

A

Stretch receptors

Walls of aortic arch and carotid sinus are able to stretch - the more they are stretch the higher the firing rate

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3
Q

Which nerves travel to the brain from the aortic arch and carotid sinus baroreceptors? Where do they lead?

A

Nerves:
Aortic via vagus nerve
Carotid via glossopharyngeal nerve

Lead to: medullary cardiovascular centres (able to correct the MAP by mechanisms previously covered)

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4
Q

What other inputs go to medullary cardiovascular centres?

A

ALL ARE FEEDBACK RESPONSE

Most important is the arterial baroreceptors
Other inputs:
cardiopulmonary baroreceptors (blood volume)
central chemoreceptors (arterial PCO2 and PO2 - respiratory drive and oxygen distribution)
chemoreceptors in muscle (metabolite concentrations)
joint receptors (joint movement)

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5
Q

What is the Valsalva manoeuvre?

A

Forced expiration against a closed glottis (trying to breathe out without letting the air out e.g. while doing a poo it increases pressure in thorax and abdomen aiding defication)

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6
Q

How does the Valsalva manouvre impact the cardiovascular system?

A

Increased thoracic pressure —> reduces filling pressure from the veins —> reduces venous return, reduces EDV, reduced SV, reduces CO, reduces MAP

Essentially blood builds up in the veins

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7
Q

What happens after performing valsalva manouvre?

A

During Valsalva manoeuvre blood builds up in the veins
After manoeuvre this floods back into heart
Venous return is restored so massive increase in SV (as preload on heart improved)
Due to massive SV baroreflex reduces heart rate and blood pressure

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8
Q

How does the kidney regulate plasma volume?

A

By making the collecting duct very permeable to water will result in lots of water reabsorption, little urine, therefore conserve plasma volume
Making collecting duct very impermeable to water will result in little reabsorption, lots of urine (diuresis), and a reduction of plasma volume

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9
Q

Which 3 hormone systems control plasma volume?

A 
Renin-angiotensin-aldosterone system 
Antidiuretic factor (ADH, vasopressin)
Atrial natriuretic peptide & brain natriuretic peptide
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10
Q

Where is renin produced?

A

Juxtaglomerular (granule cells) of the kidney

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11
Q

What triggers renin production (3)?

A

Trigger = low MAP indicated by:
Activation of sympathetic nerves to the juxtaglomerular apparatus
Decreased distension of different arterioles (renal baroreflex)
Decreased delivery of Na+/Cl- through tubule

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12
Q

What is the effect of Renin?

A

Renin converts inactive angiotensinogen —> angiotensin 1 —> angiotensin 2 by angiotensin converting enzyme (ACE)

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13
Q

What are the effects of angiotensin 2?

A

Increasing MAP by:

  • increase release of ADH from pituitary (increases water permeability of collecting duct = increasing plasma volume) + increases thirst
  • vasoconstriction (increases total peripheral resistance)
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14
Q

Where is Antidiuretic factor (ADH, vasopressin) produced and released?

A

Synthesised in hypothalamus

Released from posterior pituitary

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15
Q

What triggers production of ADH?

A

Low plasma volume and/or MAP, indicated by:

Decreased blood volume
Increase in osmolarity of interstitial fluid
Circulating angiotensin 2

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16
Q

What does ADH do (2)?

A

Increases MAP by:

Increasing permeability of collecting duct to H2O (increase plasma volume)
Causes vasoconstriction (increasing MAP)
17
Q

Where is atrial natriuretic peptide & brain natriuretic peptide produced?

A

Produced and released from myocardial cells in the atria and ventricles

18
Q

What triggers Atrial natriuretic peptide & brain natriuretic peptide?

A

Increased distension of the atria and ventricles

19
Q

What does Atrial natriuretic peptide & brain natriuretic peptide do?

A

Decreases MAP by:
Increasing exertion of Na+
Inhibit release of renin
Act on medullary CV centres to reduce MAP

20
Q

What is hypertension?

A

High blood pressure

21
Q

What are the NICE/BHS values for hypertension

A

140/90mmHg

22
Q

What is the blood pressure values for stage 1 hypertension? (Clinical & ABPM)

A

Clinic blood pressure = 140/90mmHg or higher

ABPM daytime average = 135/85 or higher

23
Q

What is the blood pressure values for stage 2 hypertension?

A

Clinic blood pressure = 160/100mmHg or higher

ABPM daytime average = 150/95mmHg or higher

24
Q

What is the risk factors of hypertension (13)?

A 
Smoking 
Diabetes Mellitus
Renal disease 
Male sex
Hyperlipidaemia 
Previous MI/stroke
Left ventricular hypertrophy 
Age (decreased arterial compliance)
Salt intake 
Alcohol intake 
High BMI 
Stress
Low birthweight 
African population (salt retainers)
25
Q

What is primary and secondary hypertension? What percentage of cases are primary vs secondary?

A

Primary hypertension = no cause found (80-90%)

Secondary hypertension = cause found (10-20%)

26
Q

How is blood pressure controlled (2)?

A

Sympathetic nervous system:
- vasoconstriction (peripheral resistance)
- reflex tachycardia (increased cardiac output)
- increase SV (increased cardiac output)
Renin-angiotensin-aldosterone system:
- maintenance of sodium balance
- control of blood volume
- control of blood pressure

27
Q

Why do we treat hypertension?

A

Number 1 medical cause of death worldwide
Reduce cerebrovascular disease by 40-50%
Reduce MI by 16-30%

28
Q

Why do we treat hypertension during pregnancy?

A

Hypertension during pregnancy is the 2nd most common cause of maternal and fetal death - complicates up to 10% of pregnancies

29
Q

What types of hypertension occur during pregnancy (3)?

A

Chronic hypertension- present before patient became pregnant (30% will develop preeclampsia)

Gestational pregnancy - hypertension which occurs during pregnancy (increased protein in urine - kidney damage)

Preeclampsia- hypertensive emergency (BP>140/90mmHg and poteinuria > 300mg/24hr)

30
Q

How is hypertension treated during pregnancy?

A

Many medications are teratogenic or fetotoxic
Pre-pregnancy planning is essential for treatment of chronic hypertension
- NOT ACE or ARB
If gestational: Nifedipine modified-release, methyl dopa, labetalol, atenolol
Preeclampsia: same as gestational PLUS intravenous: labetalol OR hydralazine OR esmolol

31
Q

What are the categories for a hypertensive emergency?

A

BP >180/120mmHg

Evidence of acute target organ failure

32
Q

What is the protocol for a hypertensive emergency?

A

Hospital admission for BP reduction
Aim to lower systolic BP by 10-20% in 1st hour then to 160/100mmHg over next 6hrs (in everyone except acute ischaemic stroke and aortic dissection) —> aggressive & rapid lowering of BP associated with increased morbidity and mortality
Start oral medication as soon as target BP achieved & ween of IV medications over 12-24hrs

33
Q

What is the ONLY indication for rapidly lowering BP in hypertensive emergency?

A

Ischaemic stroke - BP>185/110mmHg who are eligible for/or received thrombolysis within previous 24hrs OR BP>220/120mmHg in those not eligible for thrombolysis

Aortic dissection - systolic BP should be lowered rapidly to target of 100-120mmHg systolic

34
Q

What is hypertensive urgency?

A

Severely elevated BP with no evidence of acute organ damage

35
Q

What is the protocol for hypertensive urgency?

A

Patient doesn’t need admitted and can be started on dual oral therapy and assessed after 24hrs

36
Q

What is orthostatic hypotension? What are symptoms?

A

Low blood pressure when you stand up from sitting or lying down

Blood pressure decrease of 20mmHg systolic and/or 10mmHg diastolic drop within 3mins of standing

Symptoms: dizzy and light headed - may cause fainting (syncope)

37
Q

What are the risks of orthostatic hypotension?

A

Syncope along with danger of falling and risk of fractures (detrimental QOL)
Increased cardiovascular risk
Heart failure and atrial fibrillation
Increased prevalence of stroke and coronary artery disease

38
Q

What are the causes of orthostatic hypotension (5)?

A 
Ageing 
Diabetes 
Antihypertensive drugs 
Auto-immune systemic diseases 
Neurological syndromes
39
Q

Treatments of orthostatic hypotension

A

Movements which mobilise volume from lower parts of the body or stimulate pressure receptors leading to vasoconstriction
Tilt bed so patient has head up
Cold glass of weather before bed
Lack of evidence supporting preventative drugs

Cardiovascular System (37 decks)

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