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CVS > Blood pressure regulation > Flashcards

Blood pressure regulation Flashcards

1
Q

What systems are responsible for short and long term control of blood pressure?

A

short- baroreceptor reflex
mid- mechanical
long- RAAS system, sympathetic nervous system, ADH, ANP

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2
Q

Why can the baroreceptor reflex not correct sustained changes in blood pressure?

A

because the stretch threshold for firing will change and reset

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3
Q

What 3 things stimulate release of renin ?

A
  • reduced NaCl delievery to macular denser cells distal tubule (less Na+ means lower blood volume)
  • reduced perfusion to kidneys (indicates low blood volume, detected by baroreceptors in afferent arteriole
  • Sympathetic stimulation to JGA
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4
Q

Where is renin released from?

A

the granular cells of the afferent arteriole

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5
Q

What makes up the juxtaglomerular apparatus?

A
  • granular cells on afferent arteriole

- macular denser cells on distal tubule

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6
Q

What does renin do?

A

Converts angiotensinogen from liver into angiotensin 1

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7
Q

Where is ACE released from and what does it do?

A
  • from lungs

- converts angiotensin 1 into angiotensin 2

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8
Q

What are the effects of activated angiotensin 2 GPCRs?

A
  • vasoconstriction
  • aldosterone release
  • ADH release (increase water retention and thirst sensation)
  • noradrenaline release
  • increased Na+ reabsorbtion
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9
Q

What does aldosterone do?

A
  • stimulates Na+ reabsorbtion in principal cells of collecting ducts
  • by activating apical Na+ and K+ channels and Na/K/ATPase channels
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10
Q

How does ACE alone help increase blood pressure?

A

It breaks down bradykinin which is a vasodilator (so you get less vasodilation)

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11
Q

ACE inhibitors therefor can help decrease blood pressure, name an ACE inhibitor and explain why ACE inhibitors cause a dry cough?

A

ramapril (aptopril, lisinopril, perindopril, enalapril)

bradykinin accumulates causing brochoconstriction (so you cough)

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12
Q

How does sympathetic stimulation cause long term increase in blood pressure?

A
  • It decreases renal blood flow so RAAS is activated
  • stimulates the Na/H exchanger and Na/K/ ATPase pump so more Na resorbtion
  • It stimulates renin release directly
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13
Q

How does ADH increase blood pressure?

A
  • stimulates thrist sensation
  • stimulates Na/K/Cl transporter so more water reabsorbed into blood
  • stimulates vasoconstriction
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14
Q

How do the natriuetic peptides (ANP and BNP) change blood pressure?

A
  • They’re released on atrial or ventricular distension (BP too high), so aim to reduce BP
  • By vasodilation and inhibiting Na+ resorbtion
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15
Q

When are prostaglandins released and what is their effect on BP?

A
  • When angiotenisin 2 too high and acute inflammation
  • cause vasodilation and less Na+ reabsorbtion
  • cause BP to drop
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16
Q

What effect does dopamine have on BP and how?

A
  • decreases BP
  • By causing vasodilation of afferent vessels (increased perfusion deactivates RAAS)
  • Causes general vasodilation
17
Q

What is hypertension?

A

A sustained increase in blood pressure above 140/90

18
Q

What is the difference between primary and secondary hypertension?

A

primary- unknown cause (poss genetic, envromental ect)

secondary- something else is causing the hypertension (very rare)

19
Q

Name some secondary causes of hypertension

A
  • Renovascular disease- occulsion of renal artery causing decreased blood flow and so RAAS activated
  • Renal parenchymal disease- cause unclear, loss of vasodilatory substances, then water retention due to poor filtration
  • Adrenal causes
20
Q

What are the adrenal causes of hypertension?

A

conns syndrome- adenoma secretes aldosterone
cushings syndrome- high glucocorticosteroids causing Na+ and water retention
I

21
Q

Describe the impacts of hypertension

A
  • increased afterload causes LV hypertrophy (leads to heart failure) and more demand of 02 (leads to MI)
  • damages arterioles which leads to atherclerosis and weak vessels which leads to stroke, retinopathy, renal failure and aneyrism
22
Q

How can hypertension be treated non- pharamacologically?

A
  • exersize
  • diet modification
  • decreased salt intake
  • decreased fat intake
23
Q

How can hypertension be treated by drugs?

A
  • ACE inhibitors and angiotension2 receptor antagonists decrease RAAS
  • L type ca2+ channel blockers and a receptor blockers cause vasodilation
  • diuretics to decrease Na+ resorbtion and so blood volume
  • Beta blockers to decrease HR and contractability
24
Q

How can mean arterial pressure be calculated?

A 
SVx HRx TRP
or 
systolic- 1/2 (pulse pressure)
Or 
Diastolic + 1/3 ( pulse pressure)
25
Q

Define haemodynamic shock

A

Acute condition of inadequate blood flow through entire body due to massive fall in arterial pressure

26
Q

State the types of shock associated with a fall in cardiac output

A
  • cardiogenic shock
  • mechanical shock
  • hypovolaemic shock
27
Q

State the types of shock associated with a fall in TPR

A
  • distributive shock
    two types of this:
  • toxic/ septic shock
  • anaphylactic shock
28
Q

Define cardiogenic shock, state its causes and its consequences

A

Pump failure meaning ventricles cannot empty properly.
Due to MI, arrhythmias or acute worsening of heart failure.
Drop in arterial pressure means damages to kidneys, heart and brain due to poor perfusion.

29
Q

What can happen to venous pressure in cardiogenic shock?

A

Can be normal or raised- due to a back up of blood

30
Q

What mechanical shock and what causes it?

A
  • the ventricles failing to fill properly
  • Cardiac tamponade (blood/ fluid in pericardium so heart cant expand and fill properly)
  • large pulmonary embolism (RV cant empty due to back up of blood increases venous pressure, and decreased blood flow to LV causes decreased arterial pressure so ventricles cannot fill properly)
31
Q

What is hypovolaemic shock and what causes it?

A
  • a sharp drop in blood volume

- usually due to haemorrhage, severe burns, diarrhoae (severe), vomiting or loss of Na+

32
Q

What % drop in blood volume is needed for hypovolaemic shock?

A

20-30% blood loss= some signs of shock

30-40% blood loss= serious shock

33
Q

What does the body do to compensate to hypovolaemic shock?

A
  • sympathetic nervous system stimulated via baroreceptor
  • tachycardia
  • increased force of contraction and venoconstriction cause increased stroke volume
  • vasocontriction causes decreased hydrostatic pressure so net movement of fluid into blood and increase in BP
34
Q

What are the 5 key signs of hypovolaemic shock

A
  • tachycardia
  • pale skin
  • weak pulse
  • clammy extremities
  • loss of consciousness
35
Q

Why does decompensation occur in hypovolaemic shock?

A
  • tissues are damaged due to hypoxia
  • vasodilators are released due to inflammation
  • blood pressure falls more, dramatically
  • vital organs not perfused enough
  • multi system organ failure
36
Q

What is distributive shock?

A

Profound vasodilation causes a fall in TPR but the blood volume is constant.

37
Q

How does toxic/ septic shock occur?

A
  • excessive inflammatory response
  • causing vasodilator release
  • a fall in TPR
  • fall in BP causes decreased vital organ perfusion
  • also exudate forms to decrease blood volume
38
Q

What is anaphylatic shock?

A

allergic reaction causes mass histamine release causing vasodilation and fall in TPR, the CO cannot overcome this fall to compensate

CVS (7 decks)

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